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Validated All-in-One™ qPCR Primer for HIF1A(NM_001530.3) Search again
Product ID:
HQP100153
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HIF-1-alpha, HIF-1A, HIF-1alpha, HIF1, HIF1-ALPHA, MOP1, PASD8, bHLHe78
Gene Description:
hypoxia inducible factor 1 subunit alpha
Target Gene Accession:
NM_001530.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Hypoxia-inducible factor-1 (HIF1) is a transcription factor found in mammalian cells cultured under reduced oxygen tension that plays an essential role in cellular and systemic homeostatic responses to hypoxia. HIF1 is a heterodimer composed of an alpha subunit and a beta subunit. The beta subunit has been identified as the aryl hydrocarbon receptor nuclear translocator (ARNT). This gene encodes the alpha subunit of HIF-1.
Gene References into function
- hypoxic induction of the COOH-terminal transactivation domain (CAD) occurs through abrogation of hydroxylation of a conserved asparagine in the CAD
- Normoxic induction of the hypoxia-inducible factor 1alpha by insulin and interleukin-1beta involves the phosphatidylinositol 3-kinase pathway.
- Repression of alpha-fetoprotein gene expression under hypoxic conditions in human hepatoma cells: characterization of a negative hypoxia response element that mediates opposite effects of hypoxia inducible factor-1 and c-Myc.
- Review. HIF-1alpha is overexpressed in many human cancers and this correlates with disease severity. It controls expression of genes associated with angiogenesis and hypoxia resistance.
- Stabilization of hypoxia-inducible factor-1alpha is involved in the hypoxic stimuli-induced expression of vascular endothelial growth factor in osteoblastic cells
- carboxyl-terminal transactivation activity of hypoxia-inducible factor 1 alpha is governed by a von Hippel-Lindau protein-independent, hydroxylation-regulated association with p300/CBP
- up-regulates a series of genes involved in aerobic glycolysis during carcinogenesis
- activation of HIF-1 is modulated by cytochrome P-450 reductase in cell membrane
- Overexpression of HIF-1alpha and HIF-2alpha was demonstrated in three HNSCC cell lines under hypoxia and tumor tissue versus normal tissue (n = 20, HIF-1alpha, P = 0.023; HIF-2alpha, P = 0.013).
- Melphalan availability in hypoxia-inducible factor-1alpha+/+ and factor-1alpha-/- tumors is independent of tumor vessel density and correlates with melphalan erythrocyte transport
- structure of an HIF-1alpha-pVHL complex determined; role of hydroxyproline
- modulation of synthesis by sodium butyrate in colon cancer cell line HT29
- Hypoxia-inducible factor (HIF) asparagine hydroxylase is identical to factor inhibiting HIF (FIH) and is related to the cupin structural family
- crystal structure and basis for the recognition of hydroxyproline in HIF-1 alpha by pVHL.
- Inhibitors of mitochondrial complex I attenuate the accumulation of hypoxia-inducible factor-1 during hypoxia in Hep3B cells.
- Induction of leptin gene expression by hypoxia and HIF1.
- HIF-1alpha-prolyl hydroxylase: molecular target of nitric oxide in the hypoxic signal transduction pathway
- enzymatic hydroxylation of a conserved prolyl residue in hypoxia-inducible factor alpha subunits governs capture by the pVHL E3 ubiquitin ligase complex
- two sequence motifs from HIF-1alpha bind to the DNA-binding site of p53
- Human hormone-refractory prostate cancers can harbor mutations in the O(2)-dependent degradation domain.
- Data show that exposure of human colon carcinoma cells to insulin-like growth factor-1 (IGF-1) induces the expression of HIF-1 alpha, the regulated subunit of hypoxia-inducible factor 1, a known transactivator of the VEGF gene.
- Lowered oxygen tension induces expression of the hypoxia marker MN/carbonic anhydrase IX in the absence of hypoxia-inducible factor 1 alpha stabilization: a role for phosphatidylinositol 3'-kinase.
- REVIEW: Hydroxylation of specific residues in the alpha subunit of HIF by a series of non-haem iron-dependent dioxygenases as a novel mechanism of protein modification that transduces the oxygen-sensitive signal for transcription of erythropoietin
- HIF-1alpha expression related to increased angiogenesis in endometrial adenocarcinoma
- In human cancer cells, both intratumoral hypoxia and genetic alterations affecting signal transduction pathways lead to increased HIF-1 activity, which promotes angiogenesis, metabolic adaptation, and other critical aspects of tumor progression.
- These results suggest that the expression of HIF-1 and VEGF induced by Cr(VI) may be an important signaling pathway in the Cr(VI)-induced carcinogenesis.
- transactivates the human leptin gene promoter
- HIF-1 binds to Sp1 and regulates basal endoglin transcription in human and mammalian cells
- results indicate that mitochondria-derived reactive oxygen species generated in response to hypoxia and increased accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) are not necessary for oxygen sensing in HeLa cells
- Regulation of hypoxia-inducible factor 1alpha expression and function by the mammalian target of rapamycin
- Expression of hypoxia inducible factor-1 alpha and correlation with preoperative embolization of meningiomas.
- The binding of pVHL to HIF is governed by the enzymatic hydroxylation of conserved prolyl residues within peptidic motifs present in the HIFalpha family members.
- Hypoxic but not anoxic stabilization requires mitochondrial reactive oxygen species
- HIF-1alpha is regulated by hypoxia through a PGE(2)-COX-2-catalyzed pathway in human tumor cells
- autocrine regulation of TGF-beta2 production in endothelial cell hypoxia may involve cross-talk between Smad3 and hypoxia inducible factor-1alpha signaling pathways
- HIF-1 alpha is correlated with apoptosis, but has no relationship with proliferation.
- HIF-1alpha is regulated and destabilized by ARD-1 mediated acetylation.
- HIF-1alpha is regulated by the von Hippel-Lindau tumor suppressor gene product
- HIF-1 binds to FIH-1 in a specific binding site
- HIF-1alpha is activated by p38, but it does not mediate induction of VEGF mRNA
- data suggest a possible antiapoptotic role of HIF-1
- ERKs and calcium are involved in the activation in cultured hepatoma cells
- HIF-1alpha is regulated by nuclear factor kappa B during a microtubule-depolymerizing agent-induced signal cascade
- HIF-1 alpha is a target for S-nitrosation by exogenously and endogenously produced NO
- results indicate that oxidized low-density lipoprotein induced hypoxia-inducible factor-1alpha accumulation in human macrophages via a redox-mediated pathway
- MAPK signaling facilitates HIF1a and HIF2a activation through p300/CBP
- HIF-1 alpha can significantly suppress Mdm2-mediated p53 ubiquitination in vitro and blocks Mdm2-mediated nuclear export of p53
- Loss of PTEN expression and increased levels of HIF-1alpha and VEGF may play an important role in carcinogenesis and progression of colorectal adenocarcinoma.
- This protein, dominantly expressed, reduces tumorigenicity of pancreatic cancer cells through the suppression of glucose metabolism.
- Prolyl-4-hydroxylase PHD3 levels influence HIF-1 alpha stability in both normoxic and hypoxic conditions, suggesting that PHD3 may participate in a feedback loop controlling HIF activity.
- Overexpression of HIF-1alpha is associated with angiogenesis and tumor progression via regulation of VEGF in human colorectal carcinoma
- data report a novel von Hippel-Lindau tumor suppressor-interacting protein (VHLaK) that functions as a negative regulator of HIF-1alpha transactivation; findings provide a novel mechanism for the modulation of HIF-1alpha transactivation by pVHL
- ROS upregulate Rho protein expression and where active RhoA is required for HIF-1alpha accumulation during hypoxia in renal cell carcinoma cells
- Vascular endothelial growth factor gene expression in colon cancer cells exposed to prostaglandin E2 is mediated by hypoxia-inducible factor 1.
- Loss of von Hippel-Lindau protein causes cell density dependent deregulation of cyclinD1 through expression of this protein.
- hypoxia-inducible factor 1 alpha is downregulated by FOXO4 in a von Hippel-Lindau protein-independent mechanism
- hypoxia induced a biphasic effect via the PI3 kinase/AKT/GSK3beta pathway on HIF-1alpha stabilization with accumulation in early hypoxia, whereas prolonged hypoxia down-regulates HIF-1.
- role for VHL mutations promoting conventional clear cell renal cell carcinoma development by an impairment of HIF-1alpha proteolysis
- Data show that hypoxia-inducible factor 1 alpha was stabilized in the von Hippel-Lindau gene product-deficient cell line 786-0 treated with a proteasome inhibitor or cobalt ion.
- HIF-1alpha and NF-kappaB have roles in transcriptional regulation of hypoxic conditions on mast cells
- HIF1A is upregulated in rheumatoid arthritis and osteoarthritis.
- cross-talk between HIF-1alpha and Hepatitis B virus X protein may lead to transcriptional activation of HIF-1alpha target genes, which play a critical role in hepatocarcinogenesis
- Quiescent hypervascularity mediated by gain of HIF-1 alpha function.
- sequence variation is associated with VO2 max before and after aerobic exercise training in older humans
- thrombin-induced VEGF mRNA expression is associated with the regulation of HIF1A in vascular endothelial cells
- insulin cannot stabilize the HIF-1alpha protein in human and mouse cells
- HIF-1alpha is not regulated by her2/neu in Wilms tumor
- The role of HIF-1 alpha in transcriptional regulation of the proximal tubular epithelial cell response to hypoxia.
- functional requirement for HIF-1 activity was demonstrated in several different cancer cell lines, but AMP-activated protein kinase activation alone was not sufficient to stimulate the HIF-1 transcriptional activity
- HIF prolyl hydroxylase 2 is the key oxygen sensor setting low steady-state levels of HIF-1alpha in normoxia.
- signal transduction pathways involved in HIF-1alpha stabilization, HIF-1 DNA binding and transactivation by NO and hypoxia in microvascular endothelium
- S-nitrosation of the HIF-1alpha C-terminal domain by nitric oxide derived from donors and nitric oxide synthase increases protein transcriptional activity.
- role of polymorphisms in generating individually different tumor progression
- Constitutive expression of nuclear hypoxia-inducible factor-1alpha and secreted VEGF protein levels were significantly lower in IGF-IR dominant negative cells.
- Genetic variation was studied in HIF1A and there may be an association with high altitude adaptation in Sherpas.
- Overexpression of hypoxia-inducible-factor 1alpha in oesophageal squamous cell carcinoma correlates with lymph node metastasis and pathologic stage
- Hypoxia-inducible factors 1alpha and 2alpha have roles in vascular endothelial growth factor expression and in nodular malignant melanomas of the skin
- HIF-1 alpha was involved in mild hypoxia and hypoxia-mimetic CoCl2 induced leukemic cell differentiation.
- Among a panel of hypoxia-inducible genes, responses were critically dependent on Hif-1 alpha but not Hif-2 alpha in both endothelial and breast cancer cells but critically dependent on Hif-2 alpha in renal carcinoma cells.
- HIF-1alpha may play a critical role in the progression of pancreatic carcinoma.
- formation of stable protein-DNA complexes by DR/Arnt and HIF-1alpha/Arnt heterodimers with their cognate DNA sequences requires Per/Arnt/Sim A domains
- hypoxic gene induction in cells expressing HIF-2alpha but not HIF-1alpha
- regulation of HIF-1alpha by hypoxia and nitric oxide (NO) in explants of human cerebrovascular smooth muscle cells
- Control of T cell survival via the HIF-1alpha-adrenomedullin cascade constitutes a novel milieu for regulation of T cell-mediated immune response in situ.
- results have shown that the destabilization of HIF-1alpha upon inhibition of mitochondrial respiration in hypoxia is dependent on prolyl hydroxylase activity
- Both HIF-1 alpha and HK II protein expressions were co-localized in the cancer cells near necrosis, and the intensity of HIF-1 alpha protein expression was significantly correlated with HK II mRNA expression in both tumors.
- This approach supports a role of HIF-1alpha in oxygen-dependent cell cycle regulation
- Here we found that hypoxia induces MKP-1 expression in human hepatoma cells HepG2 in a time-dependent manner.
- HIF1alpha is activated by ras-induced superoxides after shockwave stimulation
- Noxa promoter responds directly to hypoxia via hypoxia-inducible factor (HIF)-1alpha.
- HIF-1a transactivation is not required for upregulation of VEGF by ionizing radiation in human glioblastoma
- PI3K/Akt contributes to HIF-1alpha stabilization by provoking expression of heat shock proteins.
- Nur77 activated by HIF under hypoxic conditions regulates production of the peptide hormone precursor POMC.
- the cooperation of HIF-1 with Sp1/Sp3 confers transcriptional activation under hypoxia to RORalpha4
- PKCzeta is responsible for the activation of HIF-alpha by inhibiting the mRNA expression of FIH-1 thus promoting the transcription of hypoxia-inducible genes.
- trans-regulation between HIF-1alpha and HIF-2alpha during hypoxia likely conveys target gene specificity
- Assessment of HIF-1 alpha expression might be useful for predicting the prognosis of pancreatic cancer patients.
- Data show that oxygen deprivation cancer cells provoked decreased mRNA and protein levels of proapoptotic Bid and Bad, and that hypoxia-inducible factor 1 (HIF-1) was dispensable for the down-regulation of Bad but required for that of Bid.
- Results show that growth factor stimulation, overexpression of Akt/PKB, or loss of PTEN resulted in enhanced expression of both HIF-1alpha and HDM2.
- Overexpression of exogenous hHIF-1alphaTe resulted in the inhibition of the endogenous HIF-1 transcriptional activity, demonstrating that the testis-specific hHIF-1alphaTe isoform is a dominant-negative regulator of normal HIF-1 activity.
- HIF-1alpha expression correlates with Mutations of VHL gene play a significant role in the tumorigenesis of renal clear cell carcinoma .
- effects of RNA interference targeting HIF-1 alpha messenger RNA on apoptosis in primary cultured human umbilical vascular endothelial cells exposed to anoxia and reoxygenation
- HIF-1alpha induces cell cycle arrest by functionally counteracting Myc.
- Data indicate that HGTD-P is a new hypoxia-inducible factor 1 alpha-responsive proapoptotic molecule that activates mitochondrial apoptotic cascades.
- Hif-1alpha is expressed in the majority of patients with node-positive breast cancer. There was significantly shorter distant metastasis-free survival & disease-free survival in patients with increased hif-1alpha expression.
- Leu-574 is essential for recruiting HIF prolyl hydroxylases, thereby providing a molecular basis for modulating HIF-1alpha activity
- Increased HIF-1alpha protein stability and enhanced HIF-1 transcriptional activity promote VEGF-A and ET-1 mediated increase of vascular permeability in donor lung grafts.
- In chronic lower limb ischemia, growth factor-1 (IGF-1) and IGF-2, were upregulated in atrophic and regenerating myocytes together with attenuated HIF, VEGF, and VEGFR-2 expression in the same cells.
- essential in changing the transcriptional response of tumours under hypoxia. It targets the transcription of over 60 genes involved in cancer biology including cell survival, glucose metabolism, cell invasion and angiogenesis.
- regulation of TGF-beta3 promoter activity by HIF-1 represents a mechanism for trophoblast differentiation during hypoxia.
- siRNA targeted degradation of HIF-1alpha and HIF-2alpha results in decreased hypoxia-induced PHD3 expression
- Increased hypoxia-inducible factor 1, alpha subunit expression is associated with endometrial carcinoma
- expression of HIF-1 alpha is increased in diverse Epstein-Barr virus (EBV)-infected type II and III cell lines, which express EBV latent membrane protein 1
- HIF-1alpha expression in esophageal cancer was significantly and negatively related to resistsance to radiation and chemotherapy.
- HIF-1alpha expression may be used to refine the prognostic information provided by grade in patients with diffuse astrocytomas
- IGF-II enhances the expression of VEGF in HaCaT cells by increasing HIF-1alpha levels.
- Inhibition of HIF-1alpha activity impairs gastric tumor growth, angiogenesis, and vessel maturation.
- upon activation by DNA damage, wt p53 mediates an accelerated degradation of HIF-1alpha protein, resulting in reduced activation of CA9 transcription and, correspondingly, decreased levels of CA9 protein
- regulation of hTERT promoter activity by HIF-1alpha represents a mechanism for trophoblast growth during hypoxia and suggests that this may be a generalized response to hypoxia in various human disorders
- HIF-1alpha and HIF-2alpha in renal cell carcinoma harboring VHL mutations do not have a major role in radiosensitivity
- By regulating HIF-1 activity and specific gene expression downstream, NF-kappaB may influence the survival threshold, with an impact on the fate of carcinoma cells after prolonged hepatocyte growth factor treatment.
- most genes tested were responsive only to HIF-1alpha siRNA, showing no effect by HIF-2alpha knock-down
- HIF1a and HIF2a are regulated by PHD1, PHD2, and PHD3
- Hypoxia-induced ID2 expression could play a significant role in the previously observed dedifferentiation of hypoxic neuroblastoma cells, which in a clinical setting could lead to less mature and more aggressive tumors.
- HDAC7 increased transcriptional activity of HIF-1alpha through the formation of a complex with HIF-1alpha, HDAC7, and p300
- M1- and M3- but not M2- or M4-AchR signals activate HIF-1 by both stabilization and synthesis of HIF-1alpha and by inducing the transcriptional activity of HIF-1alpha.
- cellular calcium chelation modulates hypoxia-inducible gene expression through activation of hypoxia-inducible factor-1alpha
- By using actinomycin D and cycloheximide we showed that A23187 induced HIF-1alpha mRNA expression.
- Nondiabetic patients had higher HIF-1alpha and VEGF expressions in myocardium compared with diabetic patients (P < 0.001).
- Results show that breast cancer development is characterized by either nuclear loss or cytoplasmic translocation of CITED4, with consequent loss of hypoxia-inducible factor-1alpha transcriptional antagonist activity.
- Sp1 has a role in Akt-mediated induction of VEGF expression through an HIF-1-independent mechanism
- Polymorphism of the HIF1A gene may confer susceptibility to renal cell carcinoma.
- HIF-1 mediates cell-autonomous activation of endothelial cells.
- Nur77 has a role in the stabilization of HIF-1alpha and in tumor progression and metastasis
- Data suggest that vascular endothelial growth factor expression is inhibited via degradation of hypoxia-inducible factor-1alpha through interference with the function of heat shock protein 90.
- pfkfb3 is a hypoxia-inducible gene that is stimulated through HIF interaction with the consensus HRE site in its promoter region
- VEGF and HIF-1alpha expression are inhibited by SU5416 through the inhibition of PI3K/AKT/p70S6K1 pathway in ovarian cancer cells
- HIF-1alpha expression resulted in increased VEGF expression and the HIF-1alpha/VEGF pathway operates in angiogenesis in chondrosarcoma
- Identification of HIF-1alpha417, a HIF-1alpha variant, which is required for transcription activity of aryl hydrocarbon receptor nuclear translocator.
- analysis of hydroxylation properties of amino acid substituted HIF-1alpha peptides
- NaB suppresses HIF-1 transcriptional activity on hypoxia-responsive genes by reducing the HRE DNA binding activity under hypoxic conditions in intestinal epithelial cells
- Hypoxia-inducible factor-1alpha (HIF-1alpha) mutation is a mechanism for enhancing HIF-1alpha activity in human prostate cancer and may increase tumor susceptibility or cause more aggressive biological behavior
- HIF-1alpha(785) may play an important role in tumor promotion mediated by the Ras oncogene, phorbol ester or tumor growth factors
- Propofol reversibly inhibits HIF-1 activity and the gene expression mediated by HIF-1 by blocking the synthesis of the HIF-1alpha subunit under 20% or 5% O2 conditions, but not under 1% O2 conditions.
- Hyperglycemia impairs hypoxia-dependent protection of HIF-1alpha against proteasomal degradation and suggest a mechanism by which diabetes interferes with cellular responses to hypoxia.
- up-regulation of RhoA induced by low-oxygen conditions may play an important role in regulation of HIF-1alpha expression in trophoblast cells.
- HP2K enhancer is an HRE consensus motif that mediates increased transcription, under hypoxic conditions, via HIF-1
- Analysis of furin promoters revealed the presence of putative binding sites for HIF-1; hypoxic/HIF-1 regulation of furin correlated with increased proteolytic activation of substrates MMP1 and TFGbeta1.
- specific association between pVHL and the hydroxylated HIF-alpha requires both the L1 and L7 loops to coordinate dynamic coupling among distant pVHL regions
- The hypoxia-inducible factor 1 is a key regulator of oxygen homeostasis in the cell.
- other mechanisms than gene amplification must be responsible for HIF-alpha overexpression at normoxia
- The HIF-1alpha ODD domain binds weakly to the isolated p53 core domain but tightly to full-length p53 to give a complex of one HIF-1alpha ODD domain with a p53 dimer.
- These results suggest a mechanistic link between succinate dehydrogenase mutations and HIF-1alpha induction.
- HIF1A is associated with angiogenesis, and expression of bFGF, PDGF-BB, and EGFR in invasive breast cancer.
- PI3K signaling is required for HIF-1alpha accumulation and VEGF synthesis
- role in expression of VEGF in cancer cells expressing her-2/neu oncogene
- a functional interaction between pRB and HIF-1alpha is confirmed by showing that HIF-1alpha reverses the transcription repressor function of pRB.
- HIF-1 expression level can be an indicator of tumor radioresistance
- Data indicate that HIF-1alpha is involved in tumorogenesis and progression of Renal cell carcinoma.
- angiotensin system system serves as a positive feedback loop and fosters pulmonary artery adventitial fibroblasts proliferation under hypoxic conditions with hypoxia-inducible factor 1 as the central effector pathway
- HIF-1alpha, STAT3, CBP/p300 and Ref-1/APE regulate Src-dependent hypoxia-induced expression of VEGF in pancreatic and prostate carcinomas
- hypoxia-inducible factor (HIF)-1 has a role in ceruloplasmin regulation
- von Hippel-Lindau tumour suppressor protein regulates HIF-1alpha and its oxygen-regulated transactivation domains at high cell density.
- Important role in maintaining tissue integrity. We confirmed ischemic crisis in ischemic colitis at molecular level, demonstrating overexpression of HIF-1 alpha and VEGF in ischemic lesions. May play important role in pathophysiology of ischemic colitis.
- HIF-1 activation induces substantial HO-1 expression that is associated with attenuated proinflammatory chemokine production by microvascular endothelium in vitro and in vivo.
- Tid-1(L) may play a critical role in pVHL-mediated tumor suppression by modulating the pVHL-dependent HIF-1alpha stability.
- Therapeutic and prognostic implication of somatic VHL alteration in renal cell carcinoma may be different according to the mutational subtype and the Pro582Ser change in HIF-1alpha may contribute to the development of metastases.
- first evidence that human hypoxia inducible factor 1alpha can be activated during physiologically relevant conditions
- Detection of HIF-1alpha protein would seem to be of value in informing the prognosis of transitional cell carcinoma of the upper urinary tract.
- Review. The role of HIF1-alpha in tumor hypoxia, its genetics, regulation, and inhibition are discussed.
- Downregulation of HIF1A promoted cell death induction and prevented activation of cellular defense by hypoxia.
- Established cells overexpressing-HIF-1alpha, and these cells produce endothelin-1 mRNA.
- Suggest that HIF-1alpha induces VEGF/ET-1/iNOS during gastric ulcer healing.
- role in motility of erythroid progenitor cells in conjuction with autocrine motility factor
- A targeted antioxidant reveals the importance of mitochondrial reactive oxygen species in the hypoxic signaling of HIF1A.
- Data supports the cyclooxygenase-2/prostaglandin E2/hypoxia-inducible factor-1alpha/vascular endothelial growth factor pathway possibly contributing to tumor angiogenesis in gastric carcinoma.
- Blocking HIF-1alpha degradation, either by saturation, or inhibition of prolyl hydroxylases or proteosomal degradation, leads to nuclear localisation of active HIF-1alpha proteins.
- under hypoxia, HIF-1alpha accumulates and transcriptionally activates its own degradation
- The transient transfection of HIF-1 alpha cDNA induced U937 cells to develop the differentiation-related alterations such as growth arrest and increased CD11b expression.
- HIF-1alpha and CA IX, but not VEGF or MMP-9, may have a role in progression of surgically resected non-small cell lung cancer
- reduction of oxygen consumption reduces the O2 gradient in conventional cell cultures, causing elevation of the cellular O2 concentration, which leads to degradation of HIF-alpha
- pvon Hippel-Lindau tumor suppressor itself is induced in prolonged hypoxia in a kinetic that parallels the observed downregulation of HIF-1alpha protein under such conditions
- Enhanced expression of HIF1A suppressed HIF2A and vice-versa.
- dysregulation of HIF-1alpha may induce the Warburg effect of aerobic glycolysis
- The lack of a hypoxia-related difference in the expression of HIF-1alpha and its target genes suggests that HIF-1alpha does not play a critical role in high altitude adaptation
- We therefore conclude that the alpha-MSH/cAMP pathway, using MITF as a signal transducer and HIF1alpha as a target, might contribute to melanoma progression.
- Results suggest an important role of stress-induced HIF-1alpha in the maintenance of chondrocyte viability in articular cartilage from osteoarthritis patients.
- In situ analyses showed that the tumours also have over-expression of hypoxia-inducible factor 1alpha (HIF1alpha) the hypothesis that increased succinate and/or fumarate causes stabilization of HIF1alpha a plausible mechanism
- Data demonstrate that ARD1 has limited, if any, impact on the HIF-1alpha signaling pathway.
- Furthermore, we determined, for the first time, that EGCG inhibits prolyl hydroxylation of HIF-1alpha, thus preventing HIF-1alpha and pVHL interaction.
- Stat3 is required for both basal and growth signal-induced expression of HIF-1
- HIF-1alpha may have a role in preventing progression of early stage squamous cell carcinomas of the oral floor
- Evidence of HIF-1 regulation of stanniocalcin-1(STC1) expression in human cancer cells. Implications as to role of STC1 in hypoxia induced adaptive responses in tumor cells.
- The review describes how activated T cells adapt to changing energy supplies in hypoxic areas of inflamed tissues by using hypoxia-inducible factor 1 (HIF1) to switch to glycolysis as the main source of energy.
- findings indicated that HIF1-alpha up-regulated expression of PDGF-B in human glioblastoma cells and showed the feasibility of siRNA technology in glioblastoma cell lines
- This review presents a model incorporating HIF-1 alpha as an oxygen sensor which regulates oxygen homeostasis and stress responsive genes in chondrocytes
- Results describe two degradation domains that differentially regulate the stability of HIF-1alpha.
- suggested that destabilization of HIF-1alpha by nitric oxide under hypoxia is under control of redox modulation; evidence provided that NO restores prolyl hydroxylase activity under hypoxia by affecting ROS production which lowers HIF-1alpha expression
- HIF-1alpha may have a role in recurrence and survival in superficial bladder cancer, while Glut-1 may have a role in survival in invasive bladder cancer
- Review of overall findings demonstrates the essential role of the hypoxia/von Hippel Lindau tumor suppressor/HIF-1 alpha pathway in endochondral bone development.
- HIF-1alpha expression in smooth muscle cells may augment vessel sprouting by loosening smooth muscle cell attachments to the basement membrane and endothelial cells
- Accumulated EGLN1 in hypoxia acts as a negative-feedback mechanism to modulate HIF-1alpha target gene expression.
- egl nine homolog 1 can be considered as a candidate tumor suppressor on chromosome 1q, and our observation could open the new aspect in exploring the machinery of senescence induction associated with HIF-1 signal transduction
- Coexpression of HIF-1alpha and CAIX in the epithelium in phyllodes tumors points to epithelial hypoxia, most probably caused by relatively distant blood vessels
- HIF-1alpha accumulation and VEGF expression could be modulated by the antioxidant enzyme MnSOD.
- Mitochondrial succinate is instrumental for HIF1alpha nuclear translocation in SDHA-mutant fibroblasts under normoxic conditions.
- Polymorphism in the HIF1A gene may confer susceptibility to androgen-independent prostatic neoplasms.
- HIF protein levels were slightly induced by acidosis and inconsistent regulation of HIF target genes under acidosis suggest additional, yet unidentified pH-sensitive factors to be involved in the regulation of these genes.
- Hypoxia-inducible factor-1alpha (HIF-1alpha) is overexpressed in many human tumors and their metastases, and is closely associated with a more aggressive tumor phenotype.
- Unexpectedly, knockdown of HIF-1alpha induced parallel knockdown of Mcl-1 mRNA and protein expression, whereas Mcl-1 knockdown had no noticeable effect on HIF-1alpha expression. The action of HIF-1alpha appeared to be mediated in part via Mcl-1.
- A3 receptor stimulation activates p44/p42 and p38 mitogen-activated protein kinases, which are required for A3-induced increase of HIF-1alpha and Ang-2
- Studies in human FaDu and HT 1080 tumor cells lines documented glucose requirement for hypoxia-induced HIF-1alpha protein accumulation
- examination of binding with mutant forms of VHL proteins
- The role of HIF-1alpha and HIF-2alpha on cell migration and proliferation in fibroblasts during hypoxia is reported.
- in pancreatic cancer cells, the p38-mediated phosphorylation of HIF-1alpha contributed to the inhibition of HIF-1alpha and von Hippel-Lindau tumor suppressor protein interaction during ischemia
- androgen receptor is involved in VEGF and hypoxia sensing via hypoxia-inducible factors HIF-1a, HIF-2a, and the prolyl hydroxylases in human prostate cancer
- HIF-1alpha and HIF-2alpha mRNA levels are transiently increased in untrained human skeletal muscle in response to an acute exercise bout, but this response is blunted after exercise training.
- We suggest, that, in addition to low oxygenation, insufficient supply of ascorbate or its excessive oxidation in tumors, can contribute to the induction of hypoxia-associated proteins via both HIF-dependent and independent mechanisms.
- ARD1 specifically binds HIF-1 alpha, suggesting a putative, still unclear, connection between these proteins.
- existence of an HIF-1alpha-bFGF amplification pathway that mediates survival and sprouting of endothelial cells under hypoxic conditions.
- Data suggest that a quadruplex structure may form in a region of the hypoxia inducible factor 1 alpha (HIF-1alpha) promoter that regulates basal HIF-1alpha expression.
- No mutations seem to occur in oxygen dependent degradation domain (ODD) of hif-1alpha in HIF-1alpha overexpressing invasive breast cancer, which rules ODD mutations out as possible explanation for diffuse HIF-1alpha expression pattern seen in this cancer
- hypoxia-elevated Ang-2 expression in gastric cancer cells may be mediated by both Cox-2-derived PGE2 and HIF-1alpha pathways
- HIF1a has a role in determining sensitivity to inhibitors of mTOR in kidney cancer
- Up-regulation of K(Ca) channels may be a novel mechanism by which HIFs can contribute to the malignant phenotype of human tumour cells.
- Coexpression of 2 VHL missense mutants (1 in the alpha domain & the other in the beta domain)restores HIF-mediated gene expression. VHL homotypic complexes target HIFalpha for ubiquitin-mediated proteolysis.
- Calpain plays an active role in degradation of HIF-1alpha.
- During hypoxia in A549 cells, HIF-1alpha promotes activity of the glycolysis pathway and decreases the pH of the culture medium, resulting in increased cellular apoptosis
- MCT4, like other glycolytic enzymes, is up-regulated by hypoxia through a HIF-1alpha-mediated mechanism
- Five antibody fragments bind within the functionally important oxygen-dependent degradation domain of the HIF-1alpha protein. Two of these antibody fragments were engineered into bivalent antibodies that were able to detect human HIF-1alpha.
- Under hypoxic conditions, the ANG and VEGF secreted by renal proximal tubular epithelial cells may modulate angiogenesis and vascular remodeling in the renal interstitium via an increase in the production of HIF-1
- In aortic vascular smooth muscle cells from humans and Zucker rats cultured in normoxia insulin increases the HIF-1alpha content in cytosol and nucleus via dose- and time-dependent mechanisms.
- HIF-1alpha was strongly expressed in ovarian cancer and may upregulate the expression of VEGF increasing tumor growth and angiogenesis
- These results show that AICAR and insulin/IGF-1 regulate VEGF expression through different mechanisms.
- These data demonstrate that HIF-1alpha knockdown reduces tumorigenicity of MCF-7 cells.
- Lipopolysaccharide induces HIF-1alpha mRNA expression & HIF-1alpha accumulation in human monocytes & in non-differentiated & differentiated THP-1 cells under normoxia. With HIF-1 activation, increase in p44/42 MAPK phosphorylation was found with LPS.
- This study demonstrated that HDAIs repress both HIF-1alpha and HIF-2alpha transactivation potential independently of von Hippel-Lindau tumor suppressor and p53 function, and indicates that HDAIs may have biological effects in a broad range of tissues.
- Normal amounts of BRCA1 function in hypoxia to regulate HIF-1alpha stability, probably by interacting with HIF-1alpha, leading to reduced levels of VEGF.
- there is an alternative mechanism for the hypoxic induction of VEGF in colon cancer that does not depend upon HIF-1alpha but instead requires the activation of PI3K/Rho/ROCK and c-Myc
- The expression level of HIF-1alpha mRNA is surmised to have a significant correlation with tumor angiogenesis, cell proliferation, apoptosis, and metastasis of pancreatic cancer.
- In hypoxia, HIF-alpha is stabilized and either dimerizes with HIF-beta to form transcriptionally active HIF for a hypoxia response, or it interacts with unrelated proteins, enabling convergence of HIF oxygen sensing with other signaling pathways.
- High expression of HIF-1alpha and VEGF-C is associated with lymphangiogenesis and invasiveness in breast cancer
- Zn chelation causes the accumulation of nonfunctional HIF-1alpha protein in both normoxia and hypoxia.
- Expression correlates with advanced disease stage, increased angiogenesis and poor prognosis in human glioma.
- Data show that during placental development, HIF1A is regulated by temporal and spatial changes in expression and association of molecules forming the multi-protein von Hippel-Lindau tumor suppressor complex as well as prolyl hydroxylase activities.
- VEGF and HIF-1alpha are elevated in malignant gliomas. HIF-1alpha inhibition results in VEGF secretion inhibition. HIF-1alpha expression affects glioma tumor growth, suggesting clinical applications for malignant glioma treatment.
- placental sFlt-1 expression is increased by both physiologically and pathologically low levels of oxygen mediated via the transcription factor HIF-1
- Expression of VEGF and Ang-2 correlated with microvessel density. Strong Ang-2 expression and/or high nuclear expression of HIF-1alpha is a significant predictive factor for recurrence after curative resection in hepatocellular carcinoma patients.
- scavenging of nitric oxide by reactive oxygen species and vice versa attenuate HIF-1alpha accumulation in a concentration-dependent manner
- HIF-1alpha function might be therapeutically targeted by inhibition of the PI 3-kinase/Akt pathway
- HIF-1alpha may play a crucial role for the survival of disc cells and resorption of the herniated disc in human intervertebral discs.
- ERK5 and ERK1/2 differ in their mechanisms of gene regulation, and ERK5 may control hypoxia-responsive genes by a mechanism independent of HIF-1alpha expression control
- differential compartmentalization of degradation of HIF-1 alpha and the subcellular distribution of HIF-1 alpha may account for cell-type-specific differences in stabilizing HIF-1 alpha protein levels under hypoxic conditions
- lower levels of HIF-1alpha in the lymph node metastases, probably induced by the less hypoxic environment, further lowered CXCR4 levels.
- hypoxia-inducible factor (HIF)-1alpha and HIF-2alpha stabilization and transactivation in a graded oxygen environment are regulated in a cell-specific manner
- The regulation of HIF by VHL plays a major role in calibration and homeostasis of the respiratory and cardiovascular systems.
- A homozygotic mutation in the von Hippel-Lindau gene that results in upregulation of hypoxia inducible factor 1alpha (HIF-1alpha) under normoxic conditions.
- HIF-3alpha, as a member of the HIF system, is complementary rather than redundant to HIF-1alpha induction in protection against hypoxic damage in alveolar epithelial cells.
- p110alpha and AKT1 play an important role in tumor growth by inducing angiogenesis and by increasing HIF-1alpha expression. This work provides a better understanding of the molecular mechanism of human cancer induced by the activation of PI3K signaling.
- A significantly greater proportion of HP75 cells transfected with siRNA targeting HIF 1-alpha mRNA sequences and exposed to hypoxia demonstrated apoptosis to a large extent when compared with non-transfected cells.
- a novel mechanism by which a growth factor controls hypoxia-inducible transcription factor-1 (HIF-1alpha) stability, and thereby drives the expression of specific genes, through the regulation of HIF-1alpha-associated prolyl hydroxylase (PHD2) levels
- Involvement of HIF-1 in uveal melanoma tumorigenesis is significant and metabolic regulation of HIF-1 activation in Mum2B uveal melanoma cells has its specificities.
- High HIF-1alpha expression is associated with head and neck cancer
- visfatin is a new hypoxia-inducible gene of which expression is stimulated through the interaction of HIF-1 with HRE sites in its promoter region.
- HIF-1alpha polymorphisms may have an important impact on HIF-protein stability and function
- Data show that activation of survivin gene expression is mediated by oxygen-independent hypoxia-inducible factor-1alpha up-regulation, mediated by epidermal growth factor (EGF) receptor signaling in EGF-treated cancer cells.
- The phosphoinositide 3-kinase (PI3K)/Akt pathway is commonly activated in cancer; therefore, we investigated its role in hypoxia-inducible factor-1alpha (HIF-1alpha) regulation.
- HIF-1alpha is a potent and rapid inducer of migration inhibitory factor expression.
- HIF-1alpha polymorpisms are an important factor for development of a subset of ulcerative intestinal tumors
- Allele C and genotypes containing this allele were associated with a higher risk of stroke in the Moscow population.
- The latency-associated nuclear antigen (LANA) directly associated with a low oxygen responder, hypoxia-inducible factor-1 alpha (HIF-1 alpha).
- Western blot analysis revealed that 2-oxoglutarate dose-dependently inhibited the HIF-1alpha protein level in Hep3B cells in hypoxic conditions.
- HIF-P4H, HIF-1alpha and HIF-2alpha are effective oxygen sensors
- This hypothesis indicates a possible novel function of heparanase and its link to HIF1alpha and Cox-2, and therefore this function would give us a clue about potential new strategies for cancer therapy.
- The HIF-1alpha immunopositivity increased through the tumor development with highest expression in the late nodular stages.
- HIF-1alpha expression in patients with breast cancer is a marker of poor therapy response and outcome, especially in ER-positive patients.
- Pseudomonas aeruginosa can recognize and respond to extracellular end products of intestinal hypoxia that are released after activation of HIF-1alpha.
- HIF-1alpha may represent an important target molecule for rrenal cell carcinoma therapy, but HIF-2alpha should be targeted in HIF-1alpha defective renal cancer cells.
- Over-expression of iNOS and HIF-1alpha in colorectal carcinoma is correlated with the biological character microvessel density.
- A rationale for targeting HIF-1 alpha with histone dacetylase inhibitors against class II isozymes as anticancer agents.
- The HIF-1alpha is considered to be a useful independent prognostic factor in gastric cancer, and the combination of a HIF-1alpha protein overexpression with nonfunctional p53 tends to indicate a dismal prognosis.
- phosphorylation of Ser-641/643 by mitogen-activated protein kinase promotes the nuclear accumulation and transcriptional activity of HIF-1alpha by blocking its CRM1-dependent nuclear export
- MTA1 enhances angiogenesis by stabilization of the HIF-1alpha protein, which is closely related to the increased metastatic potential of cancer cells with high MTA1 expression
- visfatin mRNA expression is upregulated in the fat tissue of obesity through the activation of HIF1alpha pathway due to hypoxia
- This study failed to demonstrate any prognostic significance of COX-2 expression alone or co-expression with HIF-1alpha or VEGF in advanced NPC.
- Homozygous HIF-1 alpha Pro582Ser mutation confers significant susceptibility to prostate cancer.
- demonstrated that the von Hippel-Lindau-mediated protein destruction motif of HIF-1alpha endowed procaspase-3 with hypoxia-specific cytotoxicity
- HIF-1alpha is induced by cobalt in HeLa cells by an iron-independent, but ROS-, PI-3K- and MAPK-dependent mechanism
- importance of IL-1beta-induced HIF-1alpha in regulation blood-brain barrier permeability and angiogenesis
- Hif-1alpha plays a key role in conferring apoptosis resistance under hypoxia.
- This study highlights the importance of p38 MAPK and HIF-1 in hypoxia-mediated proliferation of pulmonary artery adventitial fibroblasts.
- PHD2 induction is an underlying mechanism of NO-induced degradation of HIF-1alpha
- VHL promotes E2 box-dependent E-cadherin transcription by HIF-mediated regulation of SIP1 and snail
- HIF-1alpha expression is related to the resistance of tumor cells to chemo- and radio-therapy.
- Immunophilin-ligands FK506 and CsA suppress HIF1alpha expression by accelerating the proteasomal degradation of the protein; the suppressive effect is independent of the presence of von Hippel Lindau factor and the degree of hydroxylation of HIF1alpha.
- CXCR4 was consistently found colocalized with HIF-1alpha expression in pseudopalisading glioma cells around areas of necrosis.
- Transcriptional coordination of adenosine a2B receptor by HIF-1alpha and amplified adenosine signaling during hypoxia.
- Results describe the differential recruitment of HIF-1alpha and HIF-2alpha to common target genes in neuroblastoma, and show that HIF-2alpha promotes an aggressive phenotype.
- IL-4 induced up-regulation of HIF-1alpha gene transcription and the PI3K signaling pathway
- MUC1 attenuates HIF-1alpha activation in a survival response to hypoxic stress
- histone deacetylase inhibitors inhibit HIF activity by destabilizing HIFnd repressing its transactivation potential [review]
- activity of the alpha-subunit of the hypoxia-inducible transcription factor (HIF-alpha) are regulated by its post-translation hydroxylation as catalyzed by iron- and 2-oxoglutarate (2OG)-dependent prolyl and asparaginyl hydroxylases (PHD1-3).
- PFKFB-4 and PFKFB-3 genes are expressed in gastric and pancreatic cancer cells, they strongly respond to hypoxia via a HIF-1alpha dependent mechanism and possibly have a significant role in the Warburg effect which is found in malignant cells
- The results suggest HIF-1alpha is involved in gastric carcinogenesis and disease progression, but is only a weak prognostic factor for survival.
- HIF-1alpha gene expression was constant during early pulmonary organogenesis.
- Overexpression of HIF-1alpha is associated with breast carcinomas
- Hypoxia increases and activates myocardial HIF-1 which mediates the induction of VEGF,eNOS,p38MAP kinase and this may play a role in neovascularization,abnormal vessel formation, and cardiac remodeling.
- These results reveal that, although pericellular hypoxia may be a major contributor to HIF-1 activity, changes in the levels of soluble factors may also play a role. This study demonstrates that HIF-1 is required for CDR.
- HIF-1alpha is inhibited by NSC 644221 in a process that is topoisomerase II-dependent
- Hypoxia-inducing factor-1alpha is overexpressed in the intima of middle cerebral artery of Moyamoya patients.
- variations in HIF1alpha may play an important role in the pathogenesis and risk factor for osteonecrosis of the femoral head
- These results demonstrate that hypoxic condition-and high cell density-induced expression of Redd1 is mediated by coactivation of Sp1 and HIF-1alpha downstream of the PI3K/Akt signaling pathway.
- HIF-1a is a key factor responsible for angiogenesis by the induction of VEGF in a human osteosarcoma cell line.
- hypoxia-inducible factor-1 alpha is modulated in cultured primary cells by intracellular ascorbate
- direct regulation of HIF-1alpha stability by Glycogen synthase kinase 3 may influence physiological processes or pathophysiological situations such as metabolic diseases or tumors
- We conclude that HIF-1alpha overexpression enhances lung cancer cell invasion at least through up-regulating the expression and activities of uPAR, MMP1, and MMP2.
- Hemin induces a serum protein-sensitive pro-inflammatory phenotype in microvascular endothelial cells via an oxidant-sensitive mechanism that is powerfully regulated by HIF-1.
- induction of HIF-1alpha by atherogenic factors may be a key step in coordinating the cellular events that result in atherosclerotic lesions
- Carbon monoxide conditions the macrophages via a HIF-1alpha and TGF-beta-dependent mechanism and the earliest events in macrophage signaling that lead to and preserve cellular homeostasis at the site of injury.
- Repeated exposure to chromium can lead to extended stabilization of HIF-1alpha emphasize the important role of ascorbate in regulation of HIF-1 transcriptional activity in metal-exposed human lung cells.
- Asparagine hydroxylation and S-nitrosylation of HIF-1alpha decrease p300 binding, while its phosphorylation does not affect p300 binding, which was reconfirmed by competitive inhibition analyses using mutant peptides.
- comparison of the expression of HIF-1alpha and GLUT-1 with various clinicopathological features of colorectal cancer
- broad impact of the HIF-1 transcription factor on gene expression could make it a key regulator of UV-responsive genes and photocarcinogenesis.
- Hif-1 alpha, which is related to tissue hypoxia in endometrial cancer, is associated with overexpression of Ob and ObR (leptin and leptin receptor).
- Under conditions of reduced oxygen availability, hypoxia-inducible factor 1 reciprocally regulates COX4 subunit expression by activating transcription of the genes encoding COX4-2 and LON, a mitochondrial protease that is required for COX4-1 degradation.
- In conclusion, we provide the molecular mechanism of the cross talk between HIF-1alpha and Id-1, which may play a critical role in tumor angiogenesis.
- These results indicated that in prostate cancers, HIF-1 might cooperate with the AR to activate the expression of several genes related to tumor angiogenesis, invasion, and progression.
- Immunohistochemical expression of hypoxia-inducible factor (HIF)-1alpha in Barrett's esophagus metaplasia-dysplasia-adenocarcinoma sequence.i
- transient RNAinterference directed against HIF-1alpha can effectively curb glioma growth in vivo.
- We found that BPQ did not inhibit HIF-1alpha mRNA level, but inhibited its protein expression in a proteasome-dependent manner.
- During trophoblast hypoxia glucose transporters (GLUT1/3) are upregulated via HIF-1 alpha pathway.
- Here, we investigated the regulatory mechanism of HIF-1alpha expression by LPS in hepatocytes and identified that LPS-induced HIF-1alpha mediate gene transcription of a typical inflammatory mediator, tumor-necrosis factor alpha (TNFalpha).
- The role of protein expression of hypoxia-inducible factor (HIF)-1alpha, HIF-2alpha, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1) in patients with colorectal adenocarcinomas.
- Prostate tumor cells selected by hypoxia, normoxia or hyperoxia utilize HIF-1alpha in different ways to allow cell survival/growth.
- HIF-1alpha may induce the angiogenesis in gastric carcinoma by upregulating the transcription of VEGF gene, and take part in tumor invasion and metastasis. They can be used as prognostic markers of gastric cancer in clinical practice.
- sustained expression of HIF-1alpha can inhibit cell hyperplasia, and the apoptosis promotion of injured cells as well as provide protection of endothelial cells
- HIF-1alpha is involved in transcriptional induction of inflammatory chemokines monocyte chemoattractant protein (MCP)-1 and MCP-5 in hypoxia-stimulated astrocytes.
- There may be a hormonal and hypoxia-independent regulatory mechanism coordinating the expression of HIF-1alpha, HIV-2alpha, VEGF, the androgen receptor, and FOXP1 in prostate tumors.
- hypoxia-inducible factor 1 negatively regulates mitochondrial biogenesis and O(2) consumption in renal carcinoma cells lacking the von Hippel-Lindau tumor suppressor
- over-expression of HIF-1alpha may play an important role in pancreatic ductal adenocarcinoma progression
- HIF-1A mRNA is reduced in abundance in response to hypoxia.
- Data show that Chlamydia pneumoniae directly interferes with host cell HIF-1alpha regulation in a biphasic manner.
- Major oxygen-dependent HIF isoforms are strongly upregulated in psoriatic skin with HIF-1alpha mainly in the epidermis, in an expression pattern similar to VEGF mRNA.
- HIF-alpha proteins and regulated genes are not increased in placentas from normotensive pregnant women delivering small, asymmetrically grown babies
- shows for the first time HIF-1alpha is causally linked to the protective effects of ischemic preconditioning on endothelial cells.
- Potassium chloride may act through the calcium-independent pathway leading to enhanced HIF-1A transcriptional activity in gastric cancer cells.
- Erythropoietin may protect the kidneys against ischemia reperfusion injury by activating HIF-1alpha.
- Data show that human placental hypoxia-inducible factor-1alpha expression correlates with clinical outcomes in chronic hypoxia in vivo.(
- HIF-1alpha expression levels were significantly higher in ovarian clear cell carcinoma than in other histological types.
- Reduction of HIF1alpha levels using antimycin-A or siRNA targeting HIF1alpha did not affect PKB/Akt activation in hypoxia.
- nuclear expression of HIF-1alpha was significantly higher in stage III and IV ovarian tumors than stages I and II; cytoplasmic expression of HIF-1alpha did not show differences among histological malignancies
- SSAT2 is an essential component of the ubiquitin ligase complex that regulates hypoxia-inducible factor 1alpha
- hypoxia-inducible factor-1alpha (HIF-1alpha) and HIF-2alpha in prostate cancer has been confirmed and also immunoreactive HIF-1alpha and downstream gene products were identified in benign and malignant prostate neuroendocrine cells
- These findings provide genetic evidence that hypoxia utilizes mitochondrial reactive oxygen species as signaling molecules to activate HIF-dependent extension of replicative life span.
- Eradication of HIF-1-active/hypoxic cells in the xenografts during irradiation exhibited significant suppression in angiogenesis and strong enhancement in a long-term growth suppression of tumor xenografts.
- The hypoxia-inducible factor is stabilized in circulating hematopoietic stem cells under normoxic conditions.
- both HIF-1alpha and HIF-2alpha play important and similar roles in hypoxia-mediated stimulation of PAI-1 expression in HTR-8/SVneo cells
- HIF-1 plays a major role in tumour progression, it may represent a molecular target for the development of novel adult T-cell leukaemia therapeutics
- Overexpression of obesity hormone leptin and its receptor in human colorectal cancer appears to be associated with the abundance of hypoxia-inducible factor (HIF)-1 alpha.
- gal-3 is a HIF-1-regulated lectin that plays an important role in nucleus pulposus cell survival.
- Statistically analyzed distributions of the proteins reflected functional dependences among STAT3, HIF-1alpha, EPO and EPOR in cellular signal conduction.
- hypoxia-inducible factor 1 alpha (HIF-1alpha) alpha expression is upregulated in activated macrophages under normoxic conditions and in inflammatory atherosclerotic plaque
- HIF-1alpha demonstrates the potential to be a predictive marker for PGD
- Polymorphisms in the HIF-1alpha are not directly associated with prostate neoplasms.
- LANA can function not only as an inhibitor of HIF-1alpha suppressor proteins but can also induce nuclear accumulation of HIF-1alpha during KSHV latent infection.
- The role of HIF-1alpha protein through its nontranscriptional activity in myeloid cell differentiation.
- Increased expression of HIF-1alpha may be involved in sinusoidal capillarization and the increased numbers of unpaired arteries in capillarized areas with increased numbers of unpaired arteries in dysplastic liver nodules.
- Leptin's gene expression regulation in breast cancer is dependent on HIF-1alpha.
- PKA was shown to be involved in the phosphorylation of HIF-lalpha under intermittent hypoxia, while p42/p44 and Akt were not.
- the oxygen dependence of the prolyl hydroxylase reaction is sufficient to mediate HIF-1alpha stability under moderate as well as severe hypoxia.
- The HIF-1alpha pathway is activated in response to subepithelial remodeling and contributes to progressive premalignant epithelial lesions in the airways of tobacco smokers with chronic airway inflammation.
- bFGF augments hypoxia induced VEGF release in breast cancer cells mainly through the PI3K pathway and partly depending on HIF-1 activity.
- HIF-1alpha increased DNA-binding ability and transcriptional activity of Runx1 protein.
- KBP reduces expression of VEGF and HIF-1alpha nuclear translocation
- CREB binding to the HIF-1 responsive elements in PAI-1 promoter mediates the glucagon effect in the liver
- Substrate specificity of HIF1alpha subunit prolyl-4 hydroxylase HIF1 alpha subunit is determined by a region relatively remote from the catalytic site of the enzyme.
- Prolyl 4-hydroxylases (P4Hs) act on collagens (C-P4Hs) and the oxygen-dependent degradation domains (ODDDs) of hypoxia-inducible factor alpha subunits (HIF-P4Hs) leading to degradation of the latter.
- HIF-1 cooperates with dysregulated c-Myc to promote glycolysis by induction of hexokinase 2 and pyruvate dehydrogenase kinase 1.
- HIF-1alpha was closely linked to an aggressive phenotype in breast cancer.
- BNP is a specific HIF-1alpha target gene
- We thus propose that NDN regulates neuronal function and hypoxic response by regulating the activities of the ARNT2:SIM1 and ARNT2:HIF1alpha dimers, respectively.
- Transactivates SAG (sensitive to apoptosis gene) in response to hypoxia.
- ING4 suppression in MM cells up-regulated IL-8 and OPN, increasing the HIF-1alpha activity and its target gene NIP-3 expression in hypoxic condition
- high levels of the hypoxia regulated proteins HIF1alpha and CA9 in HNC predict resistance to platinum based radio-chemotherapy.
- SSAT1, which shares 46% amino acid identity with SSAT2, also binds to HIF-1alpha and promotes its ubiquitination/degradation. However, in contrast to SSAT2, SSAT1 acts by stabilizing the interaction of HIF-1alpha with RACK1
- conclude that the loss of iron-regulatory syste is not the course of erythrocytosis
- We conclude that edaravone inhibits VEGF expression in astrocytes exposed to hypoxia, at least partly, through the down-regulation of HIF-1alpha.
- Both the ERK pathway and the PI3K pathway are involved in the cytokine-induced HIF-1alpha expression in rheumatoid synovial fibroblasts and in the expression of proangiogenic factors
- provide a novel mechanism in which hypoxia induces HIF-1alpha mRNA expression via the phosphatidylinositol 3-kinase/AKT pathway and activation of NFkappaB
- HIF-1 activity does not require rapid proteolytic turnover of the vascular endothelial growth factor promoter-bound transactivator, nor is the activator-promoter complex constantly disassembled by chaperones
- Levels of IAP-2 and Bax were decreased in A375 cells and HIF-1alpha was increased during hypoxia.
- HIF-1 activity is necessary and sufficient for the mobilization of angiogenic cells; HIF-1alpha transgene therapy counteracts the pathological effects of aging in a transgenic mouse model of limb ischemia.
- These findings identify novel and intricate signaling mechanisms involved in HIF-1 complex activation and will lead to the elucidation of the importance of HIF-1 in different Angiopoietin II-related cell responses.
- HIF-1 may be involved in angiogenesis by controlling expression of VEGF in vivo. Possible strategy for treatment of angiogenesis by targeting HIF-1 alpha in ischemic retinopathies.
- RSUME is induced by hypoxia and enhances the sumoylation of HIF-1alpha, promoting its stabilization and transcriptional activity during hypoxia.
- that intracellular calcium levels can regulate HIF-1alpha expression by modulating calcineurin activity and RACK1 dimerization.
- differences in reactive oxygen species production, HIF proliferation, and cell proliferation contribute to the differences in tumor phenotype in cells lacking SdhB as opposed to those lacking SdhA
- HuR and PTB jointly upregulate HIF-1alpha translation in response to CoCl(2)
- identify a novel nuclear export motif, further highlight the role of nuclear-cytoplasmic shuttling of E3 ligases in degradation of nuclear substrates, and provide evidence that disease-causing mutations can target subcellular trafficking
- Inhibitory effect of 6-formylpterin on HIF1A protein accumulation is reported.
- These findings demonstrate that HIF-1alpha function is negatively affected by its interaction with MgcRacGAP.
- hypoxia-independent promotion of the AKT-HIF-1alpha-VEGF pathway contributes, at least in part, to gastric cancer tumorigenesis and angiogenesis
- An oxidative signal as a result of NO/O(2)(-) coformation triggers a calcium increase that activates calpain to degrade HIF-1alpha, independently of the proteasome.
- Review of HIFalpha proteins demonstrates that distinct prolyl hydroxylase domain proteins, including HIFalpha proteins, are remote from the catalytic site and function in substrate discrimination.
- differential expression of prolidase in 2 breast cancer cell lines showed prolidase-dependent differences in HIF-1 alpha levels
- HIF-1 alpha polymorphisms may have a significant influence on the poor prognosis of the patients undergoing radical cystectomy for bladder cancer, while they seem to have no relation to the bladder cancer occurrence
- The neurohormone orexin stimulates HIF-1 activity.
- HIF-1alpha may be an immunohistochemical marker for vasculitic neuropathy
- CCAAT/enhancer-binding protein alpha antagonizes transcriptional activity of hypoxia-inducible factor 1 alpha with direct protein-protein interaction
- HIF-1 and HIF-2 are detected in the endothelium and macrophages. Hypoxia-inducible factors in endothelial cells may induce VEGF, thereby contributing to the development of choroid neovascularization.
- VEGF, HIF-1alpha and CD34 expressions were more common in gastric tumors without serosal invasion
- In BRCA1 germline mutation related breast cancer, functional HIF-1alpha overexpression is seen at a much higher frequency than in sporadic breast cancer.
- HIF-1 alpha is expected to be useful for detection of the viability of PAs after NHT and also for prediction of their clinical outcome
- Polymorphisms in HIF1A were associated with development of stable exertional angina rather than acute MI as the initial clinical presentation of CAD.
- HIF-1alpha signaling in renal epithelial cells is associated with the development of chronic renal disease and may promote fibrogenesis by increasing expression of extracellular matrix-modifying factors and lysyl oxidase genes
- PG activates HIF-1 and enhances the resultant gene expression by directly affecting the intracellular oxygen sensing system in vitro and in vivo
- Transcription factor HIF-1alpha is involved in the up-regulation of mPGES-1 and may therefore play an important role in the metabolism of osteoarthritic cartilage.
- extracellular matrix genes are induced in dermal fibroblasts by HIF-1alpha-dependent, as well as HIF-1alpha-independent, mechanisms
- HIF-1 and HIF-2 have roles in SK1 upregulation during hypoxia in glioma cells
- We have identified a new three-gene classifier that is independent of and improves on stage to stratify early-stage NSCLC patients with significantly different prognoses.
- To our knowledge, this is the first report of differing HIF-1 activation between two strains of animals with clearly divergent physiological responses to identical hypoxic conditions.
- mitochondrial abnormalities that disturb the reactive O(2) species HIF-1alpha-Kv1.5 O(2)-sensing pathway contribute to the pathogenesis of pulmonary arterial hypertension and cancer--REVIEW
- HIF-1 alpha is an important independent prognostic factor for patients with metastatic clear cell RCC
- GLUT-1 overexpression is to some extent regulated by HIF-1alpha and is also strongly associated with histological features
- expression is an early event in oral carcinogenesis
- Studies using loss and gain of function of HIF-1 confirmed a critical role of HIF-1alpha in coordinating TLR2 and TLR6 induction
- findings support the hypothesis that the HIF-1Alpha P582S variant may confer susceptibility to subgroups of breast cancer in Korean women
- There was a significant correlation between nuclear BNIP3 expression and HIF-1alpha expression and HIF-2alpha expression but no correlation between BNIP3 and pre-operative PSA, tumor volume, margin positivity or capsular invasion.
- These results imply that HIF-1alpha functions as an up-stream player in the p21-mediated growth arrest of keratinocytes.
- mitochondria has an essential role in HIF-1 regulation
- These data suggest that HIF-1 activation of HREs within the putative chk-a promoter region can increase Chk-A expression within hypoxic environments, consequently increasing cellular PC and tCho levels within these environments.
- The protein expression of Hypoxia-Inducible Factor 1 was observed in 9 of 11 cases of cancer tissues.
- Methylation analysis of 3' enhancer showed that it was free of methylation in 70% cells in A2780, while in less than 16% in both TC1 and HeLa cells, thereby suggesting that TUBB3 increase upon hypoxia is abolished through methylation of the 3' enhancer.
- the HIF-1alpha pathway is a critical mediator of neoangiogenesis required for skeletal regeneration
- We describe a family with erythrocytosis and a mutation in the HIF2A gene, which encodes the HIF-2alpha protein. this mutation leads to stabilization of the HIF-2alpha protein and suggest that wild-type HIF-2alpha regulates erythropoietin production
- Data show that lipopolysaccharides induce HIF-1alpha activation by enhancing both protein expression and transcriptional activity in differentiated THP-1 human myeloid cells but not in undifferentiated cells.
- This study suggests that NDRG2 is a Hif-1 target gene and closely related with hypoxia-induced apoptosis in A549 cells.
- may play a role in malignant transformation of oral submucous fibrosis
- Accumulation of HIF-alpha proteins in preeclampsia placentas may occur as a consequence of both increased formation secondary to relative ischemia/hypoxia and reduced degradation after reperfusion/oxygenation consequent to proteasomal dysfunction.
- Hypoxia-induced increase in the level of HIF-1alpha in retinal pigment epithelium can be an important step in choriodal neovascularization.
- Activation of the thyroid hormone receptor beta/retinoid X receptor alpha heterodimer by T(3) stimulated expression of the hepatic leukemia factor, which increases HIF-1alpha gene expression.
- Insight into its applicability for pharmacologic targeting of HIF-1alpha for cancer therapeutic or chemopreventive purposes prostatic cancer.
- Hypoxic preconditioning of cisplatin-treated proximal tubular cells in culture reduced apoptosis in an HIF-1alpha-dependent fashion.
- AMP kinase is a key determinant of HIF-1 functions in response to reactive oxygen species and may be involffed in HIF-1 regulatory mechanisms.
- is the first case-control study that investigates the association of HIF-1alpha polymorphisms with sporadic breast cancer in the Turkish population
- A role for HIF1A as an endogenous marker of tumor hypoxia is currently not supported by the available clinical data.
- Under hypoxic conditions an autocrine loop between VEGF-C/VEGFR-3 and HIF-1 alpha is possible in breast carcinoma and lung carcinoma but not in colorectal carcinoma cell lines.
- These results imply that Pin1 stimulates VEGF expression by activating HIF-1alpha and AP-1, and suggest that Pin1 is a potential therapeutic target of angiogenesis during cancer development.
- These results suggest that MT-III upregulates VEGF production in brain endothelial cells by a HIF-1alpha-dependent mechanism.
- a key signalling pathway involving HIF-1alpha and TWIST promotes metastasis in response to intratumoural hypoxia
- Notch ICD enhances recruitment of HIF-1alpha to its target promoters and derepresses HIF-1alpha function
- role for HIF-1alpha in transcriptional repression of adenosine kinase in hypoxia
- These findings strengthen the importance of the role of PARP1 as a transcriptional coactivator of HIF-1-dependent gene expression during tumor progression.
- Suggest role for bacterial siderophores in hypoxia-independent activation of HIF-1 during infection with human pathogenic bacteria.
- Hypoxia and epidermal growth factor receptor signal coexisted in the tumor microenvironment and might promote angiogenesis through HIF-1 alpha-mediated upregulation of SCF and other angiogenic factors.
- HIF1A has a crucial role in regulating extravillous trophoblast behavior including matrigel-induced endovascular differentiation under normoxia.
- Chronic hypoxia not only increases the pool of PHDs but also overactivates the three PHD isoforms.
- Upregulation of HIF-1 alpha and its downstream targets GLUT1 and SDF-1 in colorectal adenomas and carcinomas may be due to hypoxia.
- HIF-1alpha and hypoxia play a crucial role for dendritic cell activation in inflammatory states
- HIF-1alpha expression may be regulated through HDAC1/MTA1, which is associated with a poor prognosis for pancreatic carcinoma
- HIF-1alpha may play an important role in colon cancer angiogenesis
- In endometrial cancers, no mutations of prolines P402 and P564 were found within the HIF-1alpha oxygen-dependent degradation domain.
- TXNIP is induced in response to hypoxia in a HIF-1alpha-dependent manner in pancreatic cancer cells, resulting in increased apoptosis and increased sensitivity to platinum anticancer therapy.
- Cyr61 promoted gastric cancer cell invasive ability via an HIF-1alpha-dependent up-regulation of PAI-1.
- The downregulation of ETS1 expression with small interfering RNA (siRNA) involves HIF1alpha in regulating hypoxia-inducible genes.
- These results suggest that the hypoxia induces the migration of coronary artery smooth muscle cells, and that the migration is elicited by TSP-1 of which induction is fully dependent on the stabilization of HIF-1alpha, in autocrine regulation.
- Crocidolite, dexrazoxane and hypoxia induce doxorubicin resistance in human malignant mesothelioma cells by increasing hypoxia-inducible factor-1alpha activity
- direct modulation of HIF-1alpha expression by nuclear factor kappaB
- PlGF-induced expression of ET-1 and its cognate ET-BR receptor occur via activation of HIF-1 alpha, independent of hypoxia.
- Overexpression of MnSOD in breast epithelial cells alters stabilization of HIF-1 alpha under hypoxic conditions.
- coronary artery disease patients had higher expression of HIF-1alpha (Hypoxia-inducible factor-1alpha) ;higher HIF-1alpha expression was observed in patients with collaterals compared with patients with no collaterals
- Induction of hepatocyte growth factor activator gene expression under hypoxia activates the hepatocyte growth factor/c-Met system via hypoxia inducible factor-1 in pancreatic cancer.
- COP9/signalosome increases the efficiency of von Hippel-Lindau protein ubiquitin ligase-mediated hypoxia-inducible factor-alpha ubiquitination
- inflammatory levels of NO inhibit epithelial cell migration, because of suppression of ERK1/2 signaling, and activation of HIF-1alpha and p53, with potential consequences for epithelial repair and remodeling during airway inflammation
- Nitric oxide donor, (+/-)-S-nitroso-N- acetylpenicillamine, stabilizes transactive HIF1-alpha by inhibiting VHL and asparagine hydroxylation.
- Constitutive activation of the HIF-1alpha C-transactivation domain , and not merely stabilization of the HIF-1alpha molecule, is essential for optimal HIF-mediated transcriptional and angiogenic effects.
- HIF-1alpha is an important component of the apoptotic signaling machinery in cardiomyocytes and renal epithelial cells.
- might be markers of depth of invasion or lymph node involvement. HIF-1alpha expression was a poor prognostic factor of disease recurrence or progression in patients with gastric cancers
- HIF-1alpha accumulation is able to increase level and activity of HMG-CoAR by stimulating its transcription
- HIF-1alpha protein is selectively required for down-regulation of ASK1 activated during lipopolysaccharide-induced TLR4 downstream signalling.
- In hepatitis B-related hepatocellular carcinoma,HIF-1alpha expression was found to be significantly correlated with the expression of hepatitis B virus X protein (HBx), and over-expressed HBx upregulated HIF-1alpha protein expression in vitro
- The present study suggested that the expression level of HIF-1alpha could be an independent prognostic factor in epithelial ovarian cancer.
- Antizyme suppression leads to an increment of the cellular redox potential and an induction of HIF-1alpha
- functional interdependence between MIF and HIF-1alpha protein stabilization and transactivation activity provide a molecular mechanism for promotion of tumorigenesis by MIF
- Age-dependent loss of HIF-1alpha expression and impaired wound healing in diabetic mice was corrected using electroporation of human HIF-1alpha.
- HIF-1alpha expression was shown to have no significance on survival
- Our data suggest increased HIF-1alpha expression is an important marker for metastases in osteosarcoma patients.
- Results report that oxygen deprivation can activate the autophagic pathway in human cancer cell lines via AMPK activity, independent of HIF-1, BNIP3, and BNIP3L.
- HIF-1alpha was overexpressed in OSJ. HIF-1alpha expression was correlated with tumoral microvascular density, with size, pathologic grade, and clinical stage of OSJ. Expression of HIF-1alpha was also correlated with clinicopathologic characteristics.
- HIF-1alpha target provides a new sight into the mechanisms of sulforaphane's inhibition against tumor cell proliferation
- AQP1 and HIF1 interact each other and regulate the oncogenesis of breast cancer
- Prostate cancer cells counteract the stress of prolonged serum deprivation by upregulating HIF-1 alpha protein which increases IGF-2 expression to promote cell survival.
- PCAF regulates the balance between cell-cycle arrest and apoptosis in hypoxia by modulating the activity and protein stability of both p53 and HIF-1alpha.
- HIF-1alpha can regulate MMP1 and MMP3 expressions in human bmMSCs, which might suggest a pathophysiological role of bmMSC expressing high HIF-1alpha in bone diseases.
- Measuring PDGFA, bFGF, and HIF1a expression may contribute to a better understanding of the prognosis of patients with pancreatic cancer.
- HIF-1alpha was found to inactivate the Wnt signaling by binding to hARD1 or beta-catenin, which may contribute to the hypoxia-induced growth arrest of tumor cells.
- study concludes that IFN-alpha induces the transcription of HIF-1alpha in human endothelial cells though a JAK-ISGF3 pathway under normoxic conditions, and that this response contributes to the antiproliferative activity of this cytokine
- Hypoxia-inducible factor-1alpha knockdown abolishes hypoxia-induced apelin expression.
- Hypoxia-inducible factor-1alpha overexpression alone, has no impact on the prognosis of colorectal carcinomas.
- HIF-1alpha is elevated in both TM and GBM, suggesting that although hypoxia is one of the most powerful stimuli for HIF-1alpha elevation and consequently angiogenesis, other mechanisms may cause HIF-1alpha increase in brain tumors such as TM.
- HIF-1alpha might play a crucial role in regional lymph node metastasis as a regulator of lymphangiogenesis and angiogenesis in OSCC with a possible novel pathway involving VEGF-C.
- a circuit involving c-myc, miR-17-92, and HIF-1 alpha may play a role in cancer cell proliferation under normoxia in a cellular context-dependent manner
- accumulation of HIF-1alpha in activated mast cells requires up-regulation of HIF1A gene transcription and depends on the calcineurin-NFAT signaling pathway
- These findings show a novel mode by which HIF-1alpha is regulated not only in cancer cells but also in the tumor-associated inflammatory cells, suggesting Stat3 as an important molecular target for inhibiting the oncogenic potential of HIF-1.
- In high HIF-1alpha nuclear-positive cell subpopulations, there was a significant reduction in Bid expression
- Quercetin suppressed the HIF-1alpha accumulation during hypoxia in human cancer cell lines and reduced hypoxia-induced secretion of VEGF
- Report transcriptional activation of HIF-1 by RORalpha and discuss its role in hypoxia signaling.
- Atypical CRM1-dependent nuclear export signal mediates regulation of hypoxia-inducible factor-1alpha by MAPK.
- analysis of of degradation of HIF-1alpha at normoxia that involves pVHL but is not mediated by PHDs 1-3 or by degradation boxes surrounding Pro(402) and Pro(563)
- The transcriptional activation of HIF-1 induced by hypoxia or DFO was visualized by both bioluminescence and scintigraphic reporter gene systems.
- HIF-1 alpha and Survivin are mostly expressed in invasive CRCs. Inhibition of HIF-1 alpha may lead to exploration of its potential as a diagnostic tool and possibly a target for gene therapy for colorectal carcinoma.
- Results show that many genes regulated by hypoxia and HIF-1alpha show patterns of induction with JMJD (Jumonji-domain containing)1A and JMJD2B demonstrating robust, and JMJD2C more modest, up-regulation by hypoxia.
- Results suggest that HIF1 contributes to keratinocyte migration and thus to the re-epithelialisation process by regulating laminin-332.
- increased PDK3 expression due to elevated HIF-1alpha in cancer cells may play critical roles in metabolic switch during cancer progression and chemoresistance in cancer therapy
- Hypoxic regulation of Ang-2 is HIF-dependent and demonstrate that HIF-1alpha binds in human microvascular endothelial cells (HMVEC) to an evolutionary conserved Hypoxia-Responsive Element (HRE) located in the first intron of the Ang-2 gene.
- HIF-1 alpha, a protein rapidly responsive to all-trans retinoic acid, plays a role in all-trans retinoic acid-induced differentiation of leukemic cells
- It was shown that the persons with a heterozygotic genotype of HIF-1alpha were more predisposed to the latent hypoxia development during long stay in Antarctica.
- Stable HIF-1alpha silencing enhanced hypoxia-induced cell death in vitro due to a lack of cell cycle arrest.
- UBXD7 links p97 to the ubiquitin ligase CUL2/VHL and its substrate hypoxia-inducible factor 1alpha (HIF1alpha).
- The role of hypoxia inducible factor-1 on the expression of cystic fibrosis transmembrane conductance regulator and chloride and water flux in intestinal cells is reported.
- E2-EPF UCP expression induced by growth factors or serum increased HIF-1alpha protein level under non-hypoxic conditions, suggesting that the Egr-1/SRF-UCP-VHL pathway is in part responsible for the increased HIF-1alpha protein level
- Data show that CSB mutant cells are unable to react to hypoxic stimuli by properly activating the hypoxia-inducible factor-1 (HIF-1) pathway, a defect that is further enhanced in the event of a concomitant genotoxic stress.
- Expression of HIF-1alpha in transplanted kidneys shows a significant correlation with the use of a deceased donor kidney and with cold ischemia time.
- The tubular and interstitial TGF-beta1 and HIF-1alpha expressions in chronic kidney allograft nephropathy are greater than in other groups.
- findings show that hypoxia dictates an anti-inflammatory program by driving expression of HIF-1alpha that acts to increase the number and suppressive properties of naturally occurring CD4(+)CD25(+) regulatory T cells
- Results suggest that the signals evoked by hypoxia and after ethyl-3,4-dihydroxybenzoate treatment differentially regulate HO-1 mRNA expression through HIF-1alpha-independent mechanisms.
- HIF-1alpha-regulated glycolysis module is closely related to the aggressive phenotype of hepatocellular carcinoma, and ENO1, a glycolysis module gene, might have a role in preventing metastasis
- Stem cell factor -induced accumulation of HIF-1alpha is dependent on both the PI-3-kinase and Ras/MEK/Erk pathways.
- These results suggest that CCN2 regulates the expression of VEGF at a transcriptional level by promoting HIF-1alpha activity.
- Hypoxia-associated factor, a protein expressed in proliferating cells, binds and ubiquitinates HIF-1alpha in vitro, leading to its proteasome-dependent degradation
- Data show that nitric oxide derived from S-nitrosoglutathione activates ASK1 in THP-1 human myeloid macrophages, induces accumulation of HIF-1alpha protein, and induces accumulation of p53 in normal but not HIF-1alpha knockdown THP-1 cells.
- Copper regulation of HIF1 activity is reported.
- HSP70-2 is transcriptionally upregulated by HIF-1 in cancer cells in response to hypoxia
- Sphingosine kinase 1 is a new modulator of hypoxia inducible factor 1alpha during hypoxia in human cancer cells.
- Eag1 interferes with the cellular mechanism for maintaining oxygen homeostasis, increasing HIF-1 activity, and thereby VEGF secretion and tumor vascularization
- These results confirmed that tocotrienol has an inhibitory effect on angiogenic factor secretion from cancer cells and revealed the possible mechanisms.
- expression of hypoxia-inducible factors 1 alpha and 2 alpha is dependent on mTORC1 and mTORC2
- PlGF-mediated increased FLAP mRNA expression occurred via activation of phosphoinositide-3 (PI-3) kinase, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and hypoxia inducible factor-1alpha (HIF-1alpha).
- the potential use of Hypoxia-inducible factor 1 C1772T (P582S) polymorphism and expression analysis in providing a new prognostic factor for unfavorable disease outcomes in breast cancer
- VEGF, HIF-1alpha, and predominantly PDGFRalpha are expressed in neoplastic cells in the majority of Hodgkin lymphomas.
- The sequence variants in the exon 12 of the HIF1A gene were not associated with pre-eclampsia in the Finnish population
- HIF-1alpha expression occurs in early stages of colorectal carcinogenesis and achieves a maximum in the invasive stage independent of the metastatic status.
- histone demethylases JMJD1A and JMJD2B are transcriptional targets of hypoxia-inducible factor HIF
- Results suggest that STAT3 decreases the pVHL-mediated ubiquitination of HIF-1alpha through competition with pVHL for binding to HIF-1 alpha, and then stabilizes HIF-1alpha protein levels.
- Dual role for hypoxia inducible factor 1 alpha in providing a survival or death signal, based on hypoxia duration, and consider the nuclear transcription factor, CREB, to be a possible target for hypoxic therapy against leukemia disease.
- genetic variants of HIF1A (Hypoxia-inducible factor 1-alpha )and VHL(von Hippel-Lindau tumor suppressor protein) are not associated with acute mountain sickness symptoms that occur in Sherpas at extremely high altitudes
- our study demonstrates existence of a pro-survival HIF-1alpha-dependent autocrine feedback loop in normoxic, serum-deprived prostate cancer cells
- Antisense HIF1A gene therapy enhances the therapeutic efficacy of doxorubicin to combat hepatocellular cacinoma.
- Mxi1 is an important downstream target of HIF that contributes to pVHL-deficient renal cancer tumorigenesis
- LDH5 is highly upregulated in B-cell non-Hodgkin lymphomas and is in direct relation to factor HIF1alpha and HIF2alpha expression. LDH5 expression is linked with activated VEGFR2/KDR expression
- HIF-1alpha expression is a more significant adverse prognostic factor in the tonsil than in tongue cancer.
- HIF-1alpha and HIF-2alpha have divergent roles in colon cancer
- okadaic acid promotes angiogenesis through stimulation of Akt mediated HIF-1alpha translation.
- impaired regulation of HIF-1alpha is essential for the development of diabetic wounds, and stabilization of HIF-1alpha is critical to reverse the pathological process
- HIF-alpha effects on c-Myc distinguish two subtypes of sporadic VHL-deficient clear cell renal carcinoma
- These results indicate that HDAC4 and HDAC5 increase the transactivation function of HIF-1alpha by promoting dissociation of HIF-1alpha from FIH-1 and association with p300.
- functional inactivation of HIF-alpha by stimulation of FIH-dependent p300 contributes to the YC-1-induced deregulation of hypoxia-induced genes
- nitric oxide synthase inhibitor nitro-l-arginine methyl ester further stimulated the cyclic hypoxia-driven HIF-1alpha accumulation
- Data show that EPAS1 and VEGF, but not HIF1alpha, are overexpressed in pancreatic carcinoma.
- Effect of ROS on angiogenesis in tumors expressing hot-spot p53 mutants was correlated with their ability to increase a content of HIF1 transcriptional factor responsible for up-regulation of VEGF-A mRNAs.
- An association between expression of HIF-1alpha and VEGF-D suggests that these two angiogenic factors are essential in progression of esophageal squamous cell carcinoma.
- HIF-1alpha is upregulated early in prostate cancer development with subsequent downregulation at later metastatic stages
- HIF-1alpha directly bound to the promoter of FoxM1
- HIF-1alpha-dependent repression of ENT2 increases mucosal adenosine signaling and attenuates hypoxia-associated inflammation of the intestine.
- mAKAP organized ubiquitin E3 ligases that managed the stability of HIF-1alpha and optimally positioned it close to its site of action inside the nucleus
- After treatment with everolimus, expression of p-mTOR, HIF-1alpha and VEGF was shown to be sharply depressed in clear cell adenocarcinoma
- MGr1-Ag/37LRP is actively engaged by hypoxia and represent a novel HIF-1 target.
- Overexpression of HIPK2 resulted in subsequent inhibition of HIF-1 transcriptional activity
- Rac-1 promotes pulmonary artery smooth muscle cell proliferation by upregulation of plasminogen activator inhibitor-1: role of NFkappaB-dependent hypoxia-inducible factor-1alpha transcription.
- These data suggest that hypoxia enhances the expression of MUC1 through the transcriptional regulation by HIF-1alpha in a human lung epithelial cell line.
- HIF-1 transcriptional activity and tumor-induced mobilization of circulating angiogenic cells are inhibited by anthracycline chemotherapy
- Hydronephrosis promotes expression of hypoxia-inducible factor 1 alpha.
- PGC-1alpha is coupled to HIF-1alpha-dependent gene expression by increasing mitochondrial oxygen consumption in skeletal muscle cells
- Control of HIF-1alpha expression by eIF2 alpha phosphorylation-mediated translational repression.