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Validated All-in-One™ qPCR Primer for AKT1(NM_001014431.1) Search again
Product ID:
HQP004991
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA
Gene Description:
AKT serine/threonine kinase 1
Target Gene Accession:
NM_001014431.1(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
The serine-threonine protein kinase encoded by the AKT1 gene is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq].
Gene References into function
- Binding of CTMP to PKBalpha reduces its activity by inhibiting phosphorylation on serine 473 and threonine 308.
- regulated in platelets by collage receptor glycoprotein VI
- Absence of mutations in the pleckstrin homology (PH) domain of protein kinase B (PKB/Akt) in malignant melanoma.
- Immunohistochemical localization of phosphorylated AKT/PKB in multiple myeloma cells.
- Akt enhances Mdm2-mediated ubiquitination and degradation of p53.
- Identification of 14-3-3zeta as a protein kinase B/Akt substrate.
- Phosphorylation of HDM2 by Akt, and protein binding
- IGF-I protects the cells from apoptosis by blocking the activation of caspases, which may be responsible for the loss of FAK and Akt.
- Akt promotes cell-cycle progression through the mechanisms of phosphorylation-dependent 14-3-3 binding to p27(Kip1) and cytoplasmic localization.
- AKT activation delays radiation-induced apoptosis, allowing the DNA repair mechanism more time to remove cyclobutane thymine dimers
- Different cellular localization, translocation, and insulin-induced phosphorylation of PKBalpha in HepG2 cells and hepatocytes
- This study shows that activation of Akt by pervanadate or serum is associated with tyrosine phosphorylation of Akt.
- 3' phosphoinositide lipid-dependent translocation of PKB to the plasma membrane promotes serine 473 phosphorylation, which is, in turn, necessary for PDK1-mediated phosphorylation of threonine 308 and, consequentially, full PKB activation.
- determination of high-resolution structure of the pleckstrin homology domain of bound to phosphatidylinositol (3,4,5)-trisphosphate
- connective tissue growth factor induced fibronectin production, cell migration, and cytoskeletal rearrangement are associated with recruitment of Src and phosphorylation of p42/44 MAPK and protein kinase B
- These data indicate that Akt may contribute to tumor-cell proliferation by phosphorylation and cytosolic retention of p27(kip1), thus relieving CDK2 from p27-induced inhibition.
- Data show that activation of protein kinase B (PKB)/Akt, contributes to resistance to antiproliferative signals and breast cancer progression in part by impairing the nuclear import and action of p27.
- Data show that cytoplasmic relocalization of p27(kip1), secondary to Akt-mediated phosphorylation, inactivates the growth inhibitory properties of p27(kip1) and sustains the proliferation of breast cancer cells.
- PECAM-1 involvement through Akt/PKB activation in starvation-induced transendothelial migration of CD34+CD14+ circulating precursors
- data demonstrate that Rho/ROCK pathway negatively regulates eNOS phosphorylation through inhibition of protein kinase B (PKB), whereas it downregulates eNOS expression independent of PKB
- chemotherapeutic drugs exhibited their cytotoxic effects in part by down-regulating Akt signaling following TRADD expression
- We conclude that normal HERG function in HEK293 cells requires basal activity of PKB. Our data represent the first evidence that PKB phosphorylation regulates K(+) channels.
- Decreased phosphorylation of protein kinase B and erk1/erk2 in neutrophils from patients with myelodysplastic syndrome
- This protein protects HL60 leukemia cells from TRAIL-induced apoptosis through a mechanism involving NF-kappaB activation and cFLIP(L) up-regulation.
- our data suggest that HRG-beta1, bound to the ErbB2 ErbB3 heterodimer, in the presence of membrane ER-alpha, interacts with and activates PI 3-K/Akt.
- Increased phosphorylation of this protein was observed in A431 clonal variants.
- The protein kinase Akt induces epithelial mesenchymal transition and promotes enhanced motility and invasiveness of squamous cell carcinoma lines.
- activation of Notch1 signaling mediates p53 function in HPV16 E6 and E7 cell transformation via phosphatidylinositol(PI3K)-PKB/Akt pathway
- Akt is activated by adrenomedullin
- AKT1 is regulated by JIP1
- results suggest that TRB3 promotes glucose output from liver under fasting conditions by binding to and interfering with Akt phosphorylation in response to residual insulin signaling
- Akt regulates basic helix-loop-helix transcription factor-coactivator complex formation and activity during neuronal differentiation
- phosphorylation by Akt regulates the antiapoptotic function of PED/PEA-15 at least in part by controlling the stability of PED/PEA-15
- There are clear indications of a cross-talk between PKB and important signaling molecules downstream of the T cell receptor that modulate the thresholds of thymocyte selection and T cell activation.
- Akt has a pivotal role in the regulation of endometrial cancer cell survival through the up-regulation of a specific inhibitor of apoptosis protein
- PI3K/Akt is essential for protecting human keratinocytes against UV-induced apoptosis, whereas NF-kappaB pathway provides little, if any, protective role
- The activity of p38 MAP Kinase is regulated by AKT1 in neoplasms.
- AKT is upregulated in prostate cancer and that expression is correlated with tumor progression
- protein kinase B/AKT mediates regulation of survivin levels by integrins
- AKT and MCAM are reciprocally regulated.
- Data show that inhibition of protein kinase B (PKB) involves atypical protein kinase C zeta, which physically interacts with PKB in unstimulated cells.
- dysregulation of the phosphoinositol-3-kinase/Akt pathway causes Lhermitte-Duclos disease
- AKT1 activation disrupts breast acinar architecture and enhances proliferation in an mTOR-dependent manner.
- HER2/neu predominantly uses Akt to suppress RARE binding activity, which may be one mechanism by which HER2/neu induces ATRA resistance in breast cancer cells
- Gi, but not Gq or G12/13, signaling pathways are required for activation of Akt in platelets
- AKT has a role in CXCL16 signaling that induces cell-cell adhesion and aortic smooth muscle cell proliferation
- There is a down regulation of the serine/threonine kinase, Akt/PKB, concurrent with elevated endogenous GSK3beta kinase activity in familial Alzheimer's disease beta-amyloid precursor protein expressing cells.
- the role of Akt on cell survival is mediated by XIAP
- we propose that an increased expression level of the HMGA2 protein is closely associated with the malignant phenotype in the pancreatic exocrine system.
- demonstration of a specific role for S1P3 in S1P-induced Akt activation
- results suggest that matrix metalloproteinase-1 can stimulate dephosphorylation of Akt protein and neuronal death through a non-proteolytic mechanism that involves changes in integrin alpha2beta1 signaling
- Akt negatively regulates the cell aging of endothelial cells via a p53/p21-dependent pathway.
- Data show that respiratory syncytial virus stimulates sphingosine kinase activity in lung epithelial cells, leading to activation of antiapoptotic sphingosine 1-phosphate and subsequently activation of Akt and extracellular signal-related kinase.
- Ft1 protein interacts directly with PKB, enhancing the phosphorylation of both of its regulatory sites by promoting its interaction with the upstream kinase PDK1
- role for Ins(1,3,4,5,6)P5 as a specific inhibitor of the PI 3-K/Akt signalling pathway, that may sensitize cancer cells to the action of commonly used anticancer drugs
- important role for nuclear activation of Akt 1 in thyroid cancer progression
- Thus a physiological concentration of insulin stimulated Akt-1 & Akt-2 phosphorylation in human skeletal muscle in the absence of hyperglycemia, but Akt-2 expression is impaired in muscle of obese patients with atypical diabetes with severe hyperglycemia
- These results suggest that short-term exposure to TNF-alpha augments insulin effects through protein kinase B-alpha and glycogen synthase kinase-3 beta, whereas long-term exposure causes insulin resistance in HepG2 cells.
- Expression of constitutively active PKB alpha abrogates dexamethasone stimulation of hPDK4 promoter activity.
- ET-1 enhances the ability of lung fibroblasts to contract extracellular matrix through the Akt/phosphoinositide 3-kinase (PI3-kinase) pathway to induce de novo protein synthesis of proteins that contribute to a contractile phenotype.
- Results report that a novel AMPK catalytic subunit family member, ARK5, plays a key role in tumor malignancy downstream of Akt.
- The positive regulatory role of constitutively active PKB on TCR responsiveness, subsequent T cell division, and effector function is linked to a negative regulatory mechanism on the nuclear accumulation/shuttling of NFAT and NF-kappa B proteins.
- activated Akt and Akt2 have roles in progression of pancreatic ductal adenocarcinoma
- estradiol may exert part of its proliferative and antiapoptotic effects by a nongenomic manner through the Akt signaling pathway.
- Overexpressed recombinant human AKT participates in the settings of endothelial dysfunction in SHR rats by impaired membrane localization suggesting that AKT is involved in endothelium dysfunction in hypertension.
- Data suggest that the expansion of AKT-driven prostate epithelial cells requires mTOR-dependent survival signaling and activation of hypoxia inducible factor (HIF)-1 alpha.
- T cells from hAKT1 transgenic mice had an elevated production of IFN-gamma at baseline that was maintained during sepsis, while IL-4 had little change.
- High cell density blocks EGF-dependent cell cycle progression by inhibiting EGF signaling at the level of EGF-dependent Akt activation rather than at the level of EGFR activation.
- Akt and P70S6K phosphorylation and Gadd45 levels are modulated by GPx-1 in tumor cells
- Akt1 pathway is persistently activated in head and neck squamous cell carcinoma
- Akt is required and sufficient to mediate Ang1-induced EC survival in response to growth factor depletion. Blocking Akt function abolishes angiopoietin 1 (Ang1), mediated EC survival, and activating Akt rescues a Tie2 blockade-induced EC apoptosis
- Genetic distributions of 5 single nucleotide polymorphisms studied did not deviate from Hardy-Weinberg equilibrium in patient and control groups.
- The mechanism of insulin receptor substrate-2, protein kinase B, and anti-apoptotic PKB substrate control of beta-cell growth and survival, and whether these may be targeted therapeutically to delay the onset of type 2 diabetes are reviewed.
- in primary cultures, Akt selectively phosphorylates tau at S214 rather than T212 so tau S214 may participate in Akt-mediated anti-apoptotic signaling.
- These results establish a role for FOXN1 in initiation of terminal differentiation and implicate Akt in subsequent events.
- In Goto-Kakizaki rat soleus muscle, chronic administration of antioxidant alpha -lipoic-acid partly ameliorated the diabetes-related deficit in glucose metabolism including the enzymes Akt/PKB and PI-3 kinase.
- cAMP-mediated apoptosis was largely independent of protein kinase A (PKA) and exchange protein directly activated by cAMP (EPAC), but associated with inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway
- Sp1 has a role in Akt-mediated induction of VEGF expression through an HIF-1-independent mechanism
- TNF-alpha, IL-10, and IL-6 production in Kupffer cells following LPS or lipoteichoic acid stimulation may create a basis for understanding how the balance between pro- and antiinflammatory cytokines is regulated in the liver following bacterial infection
- The rapid activation of PI3K-Akt/PKB-mTOR-p70(S6K) cascade by T3 provides a new molecular mechanism for thyroid hormone action
- demonstrated that TRAIL mediates the recruitment of PI-3K/Akt and NF-B/IB pathways in leukaemic cells, namely Jurkat T cells
- Akt kinase activity can be inhibited by a peptide spanning the betaA strand of the proto-oncogene TCL1
- Data provide evidence that Akt plays a central role in the anti-apoptotic effect of estrogen in vascular endothelial cells.
- evidence of a functional interplay among integrin receptors, PKCepsilon, and protein kinase B (PKB/Akt) in recurrent CWR-R1 prostate cancer cells
- Phosphorylated form of Akt-1 is most likely involved in the progression of prostate cancer and is an excellent biomarker for biochemical recurrence.
- The AKT1 is a susceptibility gene for Japanese schizophrenia.
- R-Ras plays a key role in cell migration by locally regulating the switch from Rac to Rho activity after membrane protrusion and adhesion
- REVIEW: negative feedback of the PI3K-Akt pathway; one feedback loop composed of mTOR and ribosomal S6 kinase blocks further activation of the pathway through inhibition of insulin receptor substrate function
- shows that breast tumor kinase interacts with protein kinase B/Akt, a serine/threonine kinase involved in cell growth and survival
- protein kinase B/Akt phosphorylation is stimulated by mechanical stretch in epidermal cells via angiotensin II type 1 receptor and epidermal growth factor receptor
- Resistin induces HASMC proliferation through both ERK 1/2 and Akt signaling pathways.
- PKB/Akt activation in response to insulin or ionizing radiation is mediated through ATM
- AKT1 regulates the cell division cycle.
- there is a negative feedback loop in apoptosis involving E2F and AKT
- These data suggest that amiloride sensitizes both tumor cells to TRAIL-induced apoptosis by promoting Akt dephosphorylation and caspase-8 activation via the intracellular acidification.
- GSK3 and PKB/Akt have roles in the integrin-mediated regulation of PTHrP, IL-6 and IL-8 in pancreatic cancer
- Gab1 tyrosine phosphorylation is stimulated by flow shear stress to mediate protein kinase B and endothelial nitric-oxide synthase activation in endothelial cells
- Akt kinase plays important survival function in T lymphocytes, which involves the regulation of FasL expression and consequent apoptotic signaling.
- activation of the PI3K/Akt pathway identified as an anti-inflammatory signal that may contribute to the establishment of Salmonella typhimurium in the intestine
- Pim-2 and Akt-1 are critical components of overlapping but independent pathways, either of which is sufficient to promote the growth and survival of nontransformed hematopoietic cells
- AKT and IL-15 may be important in extranodal NK/T-cell lymphoma tumor survival
- results show show that target of rapamycin (TOR) kinase and its associated protein rictor are necessary for AKT/PKB Ser473 phosphorylation and that a reduction in rictor or mammalian TOR (mTOR) expression inhibited an Akt/PKB effector
- there is a phosphorylation-regulated complex formation of Grb10 with 14-3-3 and Akt
- S6 kinase 1 is essential for the control of muscle cytoplasmic volume by Akt and mTOR
- S1P inhibits male germ cell apoptosis independently of its receptors, possibly by inhibiting the transcription factor NF-kappaB and Akt phosphorylation
- persistent activation of PI3K results in Akt-dependent sequestration of FoxO1 outside the nucleus of T cells interacting with APCs; this compartmentalization process can affect T cell growth after Ag recognition
- ArgBP2gamma is a physiological substrate of Akt, functions as an adaptor for Akt and PAK1, and plays a role in Akt/PAK1 cell survival pathway
- EGF and hypoxia induce CXCR4 in non-small cell lung cancer, a process regulated by the PI3-kinase/PTEN/AKT/mTOR signaling pathway and activation of HIF-1alpha
- activated Akt is positively correlated with the protein expression of the transcription/translation factor Y-box binding protein-1 (YB-1) in primary breast cancer; activated Akt binds to and phosphorylates the YB-1 cold shock domain at Ser102
- arfaptin 2 phosphorylation at Ser260 by Akt inhibits PolyQ-huntingtin-induced toxicity by rescuing proteasome impairment
- C1 domain-containing phosphatase and TENsin homologue (C1-TEN) appears to be a novel intracellular phosphatase that negatively regulates the Akt/Protein kinase B signaling cascade
- Akt activation, but not ERK1/2 activation, is required for SDF-1alpha-induced migration of epitheloid carcinoma cells
- transcriptional induction of HO-1 gene expression by AEBSF is mediated via activation of a PKB, p38 MAPK signaling pathway
- insulin induces GATA2 phosphorylation on serine 401 in a PI-3K/Akt-dependent manner, impairing GATA2 translocation to the nucleus and its DNA binding activity
- In postmortem extracts from human brain, Akt is down-regulated by a caspase-3 cleavage, establishing a progressive alteration of Akt during pathological progression of Huntington's disease.
- Differential involvement of protein kinase pathways in regulating apoptosis induction by different forms of selenium in prostate tumor cells.
- However, muscle glycogen availability appears to contribute to regulation of the Akt pathway, which may influence cellular growth and adaptation in response to resistance exercise in a low-glycogen state.
- Tumor sections frmo colorectal cancer patients showed elevated expression levels of AKT1, correlating with enhanced cytoplasmic/nuclear expression of beta-catenin.
- Thus, Akt1 contains a functional NES and mutation of the NES results in nuclear-predominant Akt1 activation that is sufficient to induce migration.
- matrix-derived mechanical forces sensed by beta1 integrin are capable of modulating ILK activity which regulates fibroblast viability via an Akt-dependent mechanism
- JIP1 and JIP3, have a cross-talk that leads to the regulation of the ASK1-SEK1-JNK signal during glucose deprivation; cross-talk between JIP3 and JIP1 is mediated through SEK1-JNK2 and Akt1.
- PKB mediates c-erbB2-induced epithelial beta1 integrin conformational inactivation through Rho-independent F-actin rerrangements.
- Cyr61 expression provides cytoprotection in hyperoxia-induced pulmonary epithelial cell death and that this effect was in part mediated via the Akt signaling pathway
- in breast cancer patients, Akt activation is associated with tumour proliferation and poor prognosis, particularly in the subset of patients with ErbB2-overexpressing tumours
- Erythropoietin stimulated Akt phosphorylation in a dose-dependent manner (1-100 U/ml).
- RET/PTC is able to phosphorylate the Y315 residue of PKB, an event that results in maximal activation of PKB for RET/PTC-induced thyroid tumorigenesis.
- Altogether, our data demonstrate that Akt1 participates in a negative regulatory feedback loop by interacting with the JIP1 scaffold protein.
- suggests that AKT plays a role in the activation of prosurvival pathways in HTLV-1-transformed cells, possibly through NF-kappaB activation and inhibition of p53 transcription activity
- activation of Akt/PKB survival pathway is caused by PDGF
- activation of SREBP-1 by Akt leads to the induction of key enzymes of the cholesterol and fatty acid biosynthesis pathways, and thus membrane lipid biosynthesis
- Study demonstrated that phosphorylated-Akt-negative and PTEN-positive expression was a predictor of survival for patients with advanced endometrial carcinoma.
- PKC412 suppresses Akt kinase activation and induces apoptosis in myeloma cell lines
- The replication of association of variants in the AKT1 gene in a family sample with similar ethnical background as in the original study adds further evidence for involvement of AKT1 in development of schizophrenic disorders.
- activation of mTOR by Akt-mediated cellular energy and inhibition of AMPK is the predominant pathway by which Akt activates mTOR in vivo
- demonstrates that attenuation of the PI3K-Akt pathway in tumors lacking TSC2 contributes to their benign nature
- overexpression of NBS1 is an oncogenic event that contributes to transformation through the activation of PI3-kinase/Akt
- in platelets glucose transport through GLUT3 is regulated by changes in surface expression and affinity modulation, which are both under control of PKB
- findings demonstrate that Akt/PKB activation was significantly elevated in cases of primary breast carcinoma with HER2/neu overexpression
- Semaphorin 4D/plexin-B1 induces endothelial cell migration through the activation of PYK2, Src, and the phosphatidylinositol 3-kinase-Akt pathway
- Introduction of a pH1 vector producing shRNA (short hairpin RNA) that targets p110beta abolished PIA [N6-(2-phenylisopropyl)adenosine]-induced Akt activation
- T-cad overexpression in vascular endothelial cells protects against stress-induced apoptosis through activation of the PI3K/Akt/mTOR survival signal pathway and concomitant suppression of the p38 MAPK proapoptotic pathway
- exogenous CXCL12 induced Akt1 phosphorylation is indispensable for proMMP-9 secretion, migration, and invasion of prostate cancer cells.
- PARP inhibition-induced Akt activation is dominantly responsible for the cytoprotection in oxidative stress
- AKT1-targeting ribozymes effective in downregulation of the isozyme and in sensitizing cells to anticancer chemotherapeutic agents
- PI3K-Akt signaling has a role in pulmonary metastatic nodule formation of osteosarcoma
- NF-kappaB1, and not c-Rel, is the critical signaling molecule downstream of the PI3K-PTEN-PKB signaling axis that regulates lymphocyte homeostasis.
- results presented in this paper provide the first direct evidence that PI3K-mediated Akt activation in adenovirus-infected corneal cells may contribute to viral pathogenesis by the prolongation of cell viability
- AKT1 is a direct target gene of Stat3 and contributes to Stat3 anti-apoptotic function
- Akt phosphorylation of acinus on serine 422 and 573 results in its resistance to caspase cleavage in the nucleus and the inhibition of acinus-dependent chromatin condensation.
- Caveolin-1 is more expressed in cancer tissues than normal colon and related with Akt-1, not with Epidermal Growth Factor Receptor expression in colorectal cancer tissues, which suggests that signaling for caveolin-1 affects Akt-1 activation.
- PGC-1alpha gene expression is down-regulated by Akt- mediated phosphorylation and nuclear exclusion of FoxO1 in insulin-stimulated skeletal muscle
- Akt was rapidly phosphorylated by glimepiride and antisense oligonucleotides directed to Akt completely inhibited glimepiride-induced NO production. These data demonstrate that glimepiride induces NO production in HCAECs by activating PI3-kinase and Akt.
- Novel role for Akt phosphorylation in regulating the late stages of exocytosis and suggest which is achieved byphosphorylation of cysteine string protein on serine 10.
- There is constitutive activation of Akt in the majority of primary human lymphomas and hematopoietic cell lines which support its proposed key role in lymphoma cell survival.
- CKIepsilon-induced down-regulation of PI3K/Akt signaling through PTEN leads to amplified sensitivity to apoptosis.
- XIAP expression in colorectal cancer is regulated by hepatocyte growth factor/C-met pathway via Akt signaling
- Ser(87) of Bim(EL) is an important regulatory site that is targeted by Akt to attenuate the pro-apoptotic function of Bim(EL), thereby promoting cell survival
- Ang II increases albumin endocytosis through an AT(2) receptor mediated by activation of PKB in the plasma membrane, which depends on the basal activity of the phosphatidyl-inositol 3-kinase.
- In this study, we provide evidence for isoform-specific positive and negative roles for Akt1 and -2 in regulating growth factor-stimulated phenotypes in breast epithelial cells
- Akt activation may be involved in cell survival and extracellular matrix remodelling in human endometrium and decidua.
- Protein kinase B signaling pathways mediate CD36 expression in response to oxidized low density lipoprotein (oxLDL).
- Results suggest that the antiapoptotic effects of erythropoietin in neuronal cells require the combinatorial activation of multiple signaling pathways, including STAT5, AKT, and potentially MAP kinase.
- Data report that cepharanthine induces apoptosis in HuH-7 cells through activation of JNK1/2 and the downregulation of Akt.
- Activation of Rac by heregulin beta1 is mediated not only by ErbB3 and ErbB2 but also by transactivation of EGFR, and it is independent of ErbB4.
- Both activation of JNK and inhibition of Akt play a role in translocation of Nur77 from the nucleus to the cytoplasm.
- Data suggest that endothelial activation of Akt suppresses lesion formation via increased NO production, preservation of functional endothelial layer, and suppression of inflammatory and proliferative changes in the vascular wall.
- data show that inhibition of PI3K/protein kinase B (PKB) increased endostatin-induced apoptosis, and that endostatin-induced cell death is physiologically linked to PKB-mediated cell survival through caspase-8.
- hAR is a direct target of LEF-1/TCF transcriptional regulation in PCa cells; expression of the hAR protein is suppressed by a degradation pathway regulated by cross-talk of Wnt, Akt, and PP2A
- acute UV exposure downregulates TSP1 expression via PI3K-Akt activation in human keratinocytes
- CARMA1 complex is required for induction of NF-kappaB by Akt, Akt plays a modulatory role in NF-kappaB induction
- 14-3-3sigma stabilizes p27 Kip1 by inhibiting the activity of PKB/Akt
- reactive oxygen species generated by Nox4, at least in part, transmit cell survival signals through the AKT-ASK1 pathway in pancreatic cancer cells and their depletion leads to apoptosis.
- Overexpression of TSC2 rescues the migration phenotype of myr-Akt1-expressing tumor cells, and high levels of TSC2 in breast cancer patients correlate with increased metastasis and reduced survival.
- The activation and regulation of Akt and NF-kappa B in prostatic cancer cell line 1-LN are reported.
- Akt regulates its kinase activity through autophosphorylation
- VCP is an essential target of Akt signaling
- These results indicate that tryptase can activate PI3K-PKB pathway and enhance IL-8 expression.
- BAF155 and potentially INI1 are substrates for Akt phosphorylation
- The data support the significance of regulated Rac signaling in mediating Schwann cell-axon interaction and suggest that controlling Rac activity as a possible therapy for schwannomas.
- Findings did not confirm the association of AKT1 SNP2/3/4 TCG haplotype with the risk of schizophrenia, but showed the evidence of association with a different haplotype, AKT1 five-SNP AGCAG haplotype, with the risk of schizophrenia in Iranian population
- angiostatins K1-3, K1-4 and K1-4.5 mediate anti-angiogenesis in a process involvingp53, FasL, AKT and mRNA deregulation
- It was found that an active process mediates AKT nuclear translocation as shown by fusing AKT with GFP3 protein.
- PI3K/AKT, MAPK/ERK and NFkappabeta signalling have roles in the maintenance of human embryonic stem cell pluripotency and viability
- These results suggest a critical role for the CS amplitude and the balance between Rac and Rho in mechanochemical regulation of lung EC barrier.
- C5b-9 regulation of the cell cycle activation in aortic endothelial cells through Akt pathway is dependent on inactivation of FOXO1
- Overexpression of dominant-active Akt1 restored HIF-1alpha expression
- The O-GlcNAc-modification on Akt1 may play a role in Akt1 nuclear localization.
- LRRC4 plays a major role in suppressing U251 cell proliferation by regulating the extracellular signal-regulated kinase (ERK)/Akt/NF-kappaBp65, STAT3, and JNK2/c-Jun pathways.
- results demonstrate that PI3-K/Akt pathway is activated constitutively in Burkitt's lymphoma cell line, P3HR-1; it promotes cell growth and the lytic cycle cascade of Epstein-Barr virus downstream of ZEBRA
- Data show that inorganic phosphate controls cell growth by activating ERK1/2 cascades and by facilitating the translocation of Mnk1 from cytosol into nucleus through an Akt-mediated MEK pathway.
- PYK2 mediates anti-apoptotic AKT signaling in response to benzo[a]pyrene diol epoxide in mammary epithelial cells
- AKT1 play an important role in tumor growth by inducing angiogenesis and by increasing HIF-1alpha and VEGF expression. This work provides a better understanding of the molecular mechanism of human cancer induced by the activation of PI3K signaling.
- PKCepsilon activates Akt via DNA-PK to mediate its antiapoptotic function
- Acidic pH exposure protects HEMEC through induction of Hsps and activation of MAPK and PI3 kinase pathway.
- The functional response of mesangial cells to treatment with CTGF was associated with the phosphorylation of Akt/protein kinase B (PKB) and resultant phosphorylation of a number of Akt/PKB substrates, including FKHR and p27(Kip-1).
- Akt activation was detected at very early, prenecrotic stages of disease pathogenesis, and maximal activation was observed during peak stages of muscle hypertrophy.
- The Akt expression pathway is marker of outcome in glioblastoma.
- Akt-and CREB-mediated prostate cancer cell proliferation is inhibited by Nexrutine, a Phellodendron amurense extract
- Results describe the roles of MEK1/ERK and AKT/PKB pathways on the effects of granulocyte macrophage colony-stimulating factor (GM-CSF) and M-CSF on tumor progression of lung cancer.
- Akt overactivation prevents the nuclear translocation of ERK1/2 and the AngII-induced proliferation through interaction with and stabilization of endogenous PEA-15.
- Inhibition of AKT1 is sufficient to affect cell migration, invasion, and proliferation.
- HO-1 and Akt exert codependent cytoprotective effects against oxidative stress-induced apoptosis in human aortic smooth muscle cells.
- SHIP2 substitutes for PTEN in the acute regulation of PKB in PC3 cells but not other prostate cell lines, where PTEN may share this role with further PIP3-degrading mechanisms.
- Hsp90 inhibition transiently activates Src kinase and promotes Src-dependent p85 PI3K and Akt and Erk activation
- 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.
- Akt regulates nuclear/cytoplasmic localization of tuberin.
- P-Akt expression also provides a potential mechanistic link between these pediatric tumors and adult malignancies.
- Leptin stimulates proliferation and inhibits apoptosis in colon cancer cells. This effect involves JAK2, PI3 kinase and JNK and activation of the oncogenic transcription factors signal transducer and activator of transcription
- We demonstrate, for the first time in human skeletal muscle, that the regulation of Akt and its downstream signalling pathways GSK-3beta, mTOR and Foxo1 are associated with both the skeletal muscle hypertrophy and atrophy processes.
- histone deacetylase inhibitors not only inhibit deacetylase activity but also stimulate active NF-kappaB transcription and cell survival through signaling pathways involving Akt and increased p300 acetyltransferase activity
- AKT-induced BAD phosphorylation and its subsequent cytoplasmic sequestration by 14-3-3zeta is a major mechanism responsible for the postponement of UVB-induced apoptosis in human keratinocytes.
- Akt in thyroid tumorigenesis.
- Cross-talk between AKT and estrogen receptor beta-mediated transcription pathways may represent an important aspect that may influence breast cancer response to endocrine therapy.
- Results reveal that the SIN1-rictor-mTOR function in Akt-Ser473 phosphorylation is required for TORC2 function in cell survival but is dispensable for TORC1 function.
- Data show that UVB irradiation increases PTEN/Akt phosphorylation in dermal fibroblasts, and inhibition of PTEN and activation of Akt by phosphorylation are involved in UVB-induced MMP-1 and -3 secretions through upregulation of AP-1 activity.
- The cAMP-stimulated inverse ROS response in granulocytes from type 1 and type 2 diabetic patients may be due to a change in signaling pathways from cAMP/protein kinase A to PKB.
- These data suggest that IGF-1R and PKCdelta are required to stimulate PKB phosphorylation in response to BMOV in HepG2 cells.
- The data suggest that in response to hydrogen peroxide, two pathways are activated in Jurkat T lymphocytes that converge to result in the phosphorylation of Akt on S473 and T308.
- This study fails to support reduced signaling of the AKT-GSK3beta molecular cascade in schizophrenia.
- Akt activity decreases dramatically during the course of neutrophil death.
- analysis of the LLKIL motif in CXCR2, which is required for full IL-8 ligand-induced activation of Erk, Akt, and chemotaxis in HL60 cells
- We showed Akt activation to significantly correlate with HER2 overexpression or LOH at the PTEN gene locus while inversely correlating with the PR expression.
- vascular endothelial growth factor expression is induced through the glucocorticoid receptor-related phosphatidylinositol 3-kinase/Akt and beta-catenin/T-cell factor-dependent pathway in human endothelial cells
- Akt1 and Akt2 have opposing roles in Rac/Pak signaling and cell migration
- impaired cell cycle and death sensitivity, are explained by a specific defective activation of Akt that impairs the expression of Survivin
- AKT prevents VEGF during internl ribosome entry site activity in myeloma cells during mTOR inhibition.
- the primary signaling pathway for LPC-dependent dendrite formation in human melanocytes involves the activation of PKCzeta and PKCzeta phosphorylation is Rac dependent
- using akt1, the evidence is supported that akt signalling plays a significant role in the chemoresistant phenotype in glioma
- In organotypic culture, AKT mediates changes related to cell shape and size with an expansion of the differentiated compartment.
- Mice transfected with human AKT1 modified with myristoylation show increases in the susceptibility of these mice to the induction of mammary tumors of epithelial origin by the carcinogen DMBA.
- S6K1 regulates GSK3 under conditions of mTOR-dependent feedback inhibition of Akt
- chemoattractant-stimulated superoxide production can be amplified by a positive feedback loop in which p67(phox) targets Vav1-mediated Rac activation
- Luteolin inhibits IGF-1R/AKT signaling, these results provideing a new insight into the mechanisms that luteolin inhibits testicular cancer cells.
- phosphorylation is a mechanism for regulation of insulin receptor substrate-1/2, Akt, and ERK1/2
- These data identify actin as a new functional target of Akt signaling.
- Akt activation is not associated with differences in survival or smoking status in bronchioalveolar carcinoma.
- The current data suggest that, following exposure to zinc, the sequential activation of Akt and GSK-3beta plays an important role directing hippocampal neural precursor cell death.
- Novel c-Akt-regulated genes contributing to Scatter factor-mediated antineoplastic drug resistance.
- TGF-beta1 co-ordinately and independently activates the FAK and AKT protein kinase pathways to confer an anoikis-resistant phenotype to myofibroblasts.
- inhibition of ITD/Flt3 activity did not prevent the phosphorylation of ERK, STAT5 or Akt in some primary AML cells. In parallel, in these cells, Flt3 and ERK or Akt cooperate to regulate cell survival
- These data reveals for the first time that PDK1 and PKB may differentially activate NF-kappaB, and that TPCK may subserve a useful anti-inflammatory function by inhibiting IKKbeta.
- These results indicate that increased hexosamine biosynthetic pathway flux in human astroglial cells results in a rapid, short-term phosphorylation of Akt that is likely a result of increased endoplasmic reticulum stress.
- Results show that coculture with ECs enhances VSMC adhesion and spreading by up-regulating beta(1)-integrin expression and activating the PI3K/Akt pathway. Interaction between ECs and VSMCs serves a role in vascular homeostasis and remodeling.
- Akt1 is a critical regulator of dendritic cell (DC) lifespan, and its manipulation in DCs can improve the clinical efficacy of DC-based tumor vaccines
- A novel function of the AKT pathway is demonstrated in prostate cancer progression; constitutively active AKT promotes neuroendocrine differentiation and dominant negative AKT inhibits it.
- Myxoma virus (MV) M-T5 host range protein is functionally interchangeable with the host PIKE-A protein and that the activation of host Akt by either M-T5 or PIKE-A is critical for the permissiveness of cancer cells for MV.
- VEGF-A, STAT5 and AKT are downregulated in acute myeloid leukemia blasts of patients treated with SU5416
- Treatment with oleandrin facilitated nuclear translocation of FKHR in human, but not murine cells by dephosphorylating Akt.
- hypoxia-mediated suppression of Akt may induce caspase-mediated IRS-1 cleavage
- In sum, using a quantitative approach to study Akt activation identified ligand-dependent limits for the use of T308 or S473 as proxies for kinase activity.
- PI3K/Akt activation may lead to the development of chemoresistance in AML blasts through a mechanism involving a p53-dependent suppression of MRP1 expression.
- These data indicate that the aberrant expression of PTEN contributes to the activation of the PI3kinase/Akt pathway and its transcription factor mediators in glioma.
- protein kinase B, LKB1, and AMP-activated protein kinase have roles in activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes
- Akt2 was unable to induce CREB phosphorylation at Ser-133 in vivo and CREB target gene expression.
- Akt/Bad pathway generates a progressive resistance to apoptosis, at a time HTLV-I genes expression is silenced.
- These results indicate that resveratrol seems to exert its growth-inhibitory/apoptotic effect on the breast cancer cell line MCF7 via the Akt-caspase-9 pathway.
- 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.
- siRNA constructs of AKT1 may effectively down-regulate the expression of AKT1 and reverse the resistant phenotype of gastric cancer cells
- results delineate a novel force-activated inside-out Src/PI3K/FAK/Akt pathway by which cancer cells regulate their own adhesion.
- The data suggest that aberrant activation of PI3K/Akt pathway plays an extensive role in thyroid tumorigenesis, particularly in FTC and ATC, and promotes progression of BTA to FTC and to ATC as the genetic alterations of this pathway accumulate.
- Akt thus serves as a molecular switch that increases angiogenesis and the generation of superoxide, fostering more aggressive tumor behavior.
- This study demonstrates a cachexia-associated loss of Akt-dependent signalling in human skeletal muscle with decreased activity of regulators of protein synthesis and a disinhibition of protein degradation.
- Par6alpha-mediated inhibition of insulin-dependent glycogen synthesis in C2C12 cells depends on the direct interaction of Par6alpha with aPKC and on aPKC-mediated T34 phosphorylation of Akt1.
- Our findings suggest HMGA1 promotes anoikis resistance through a PI3-K/Akt-dependent mechanism.
- We conclude, therefore, that estrogen opens BK(Ca) channels in HCASMC by stimulating nNOS via a transduction sequence involving PI3-kinase and Akt.
- advances in the understanding of TCL1-Akt functional interaction in order to clarify the biological action of the proto-oncogene TCL1 family {review]
- Elevated and highly expressed levels in both laarge B-cell lymphoma and Hodgkin lymphoma.
- study provides at best weak support for the hypothesis that AKT1 is a susceptibility gene for schizophrenia
- Mechanism to selectively terminate Akt-signaling pathways through the differential inactivation of specific Akt isoforms by specific PHLPP isoforms.
- It was demonstrated that activation of phosphatidylinositol 3-kinase (PI3K) and Akt1 facilitated the nuclear translocation of Akt1, but the phosphorylation at threonine 308 and serine 473 was not prerequisite.
- These results indicate that the phosphatidylinositol 3-kinase/Akt/FoxO1 pathway participates in Ang II suppression of hSR-BI/CLA-1 expression and suggests that the endothelial receptor for hSR-BI/CLA-1 is downregulated by the renin-angiotensin system.
- receptor and nonreceptor PTKs have roles in modulating H2O2-induced ERK1/2 and PKB signaling [review]
- These findings implicate Akt in upstream events leading to BRCA1 nuclear localization and function.
- Fak/Src signaling to the PI3-K/Akt-1 and MEK/Erk pathways undergoes a differentiation state-specific uncoupling in enterocytes.
- KGF triggers negative feedback between ERK1/2 and AKT pathways to regulate cell proliferation/differention.
- These results indicated that the activation of CXCR4 and its signaling pathways (MEK1/2 and Akt) are essential for CXCL12-induced cholangiocarcinoma cell invasion.
- NF-kappa-B inhibition enhances CASP3 degradation of Akt1 and apoptosis in response to campothecin.
- PI3K/ILK/Akt/NF-kappaB axis is a promising target for therapeutic intervention in renal cell carcinoma.
- Lipid raft cholesterol regulates apoptotic cell death in prostate cancer cells through EGFR-mediated Akt and ERK pathways.
- IGF-1 rescue of AR toxicity is diminished by alanine substitutions at the Akt consensus site
- PKB/Akt inhibits ceramide-induced apoptosis in neuroblastoma cells by blocking AIF translocation.
- Proinvasive activity of BMP7 through SMAD4/src-independent and ERK/Rac/JNK-dependent signaling pathways in colon cancer cells is reported.
- vascular endothelial growth factor by Akt and mammalian target of rapamycin inhibitors in cell lines derived from childhood solid tumors
- Results show a a significant correlation between the EGFR L858R mutation and the expression of p-Akt and suggest that the activation of Akt is dependent on EGFR mutation pattern.
- In normal human skin, phospho-Akt appeared in the basal epidermal layer, but in psoriasis, phospho-Akt expression was low in the epidermis.
- EGFR/Akt pathway mitigated G2/M arrest in human HaCaT keratinocytes and normal human keratinocytes treated with low doses of UVA irradiation.
- Data show that Chlamydia trachomatis activates Rac and promotes its interaction with WAVE2 and Abi-1 to activate the Arp2/3 complex resulting in the induction of actin cytoskeletal rearrangements that are required for invasion.
- Activation and phosphorylation of the extracellular signal-regulated kinase 1/2 and AKT pathways are involved in cervical adenocarcinoma metastases to pelvic lymph nodes.
- Rho inactivation allows the activity of Rac to become dominant leading to stimulation of the phosphoinositide 3-kinase/Akt/IkappaB kinase/nuclear factor-kappaB prosurvival pathway.
- The AKT signaling pathway was directly involved in the effects induced by siRNA targeting LMP1.
- Incubation in the presence of Remnant lipoproteins (TG-rich lipoproteins )for 48 h induced the proliferation of prostate cancer PC-3 cells more significantly than prostate cancer LNCaP cells and human prostate stromal cells
- there is a link between Akt activation, repair of DNA damage, and radioresistance in glioblastoma
- Effects of endurance exercise training on insulin signaling and AKT in human skeletal muscle
- IGF-1 regulates ether-a-go-go channel activity in breast neoplasms, via an Akt pathway to promote cell proliferation.
- Tiam1-deficient lymphomas showed increased Rac activity, suggesting that the lack of Tiam1 is compensated by alternative Rac-activating mechanisms that lead to increased progression of PI3-kinase-induced T-lymphomas.
- 3,3'-diindolylmethane -induced cell growth inhibition and apoptosis induction are partly mediated through the regulation of Akt/FOXO3a/GSK-3beta/beta-catenin/AR signaling
- Reduced activation of NF-kappaB via impaired PI3K/Akt activation under increased TNF-alpha levels could result in increased apoptosis of vitiliginous keratinocytes.
- Akt1 is cleaved in vitro at the caspase-3 consensus site DQDD(456; Resistance to cleavage at site DAKE(398) (within the kinase domain) in response to phosphorylation suggests a possible mechanism by which the anti-apoptotic role of Akt1 is regulated.
- PKB/Akt may regulate specific cellular responses to growth factors such as insulin under adverse conditions such as hypoxia
- Gastrointestinal stromal tumor secondary KIT mutations can be associated with KIT hyperactivation and imatinib resistance, in which AKT PI3-kinase is a crucial survival pathway.
- Phosphorylated Akt activity is associated with invasive ductal carcinoma of the breast.
- Results suggest that aberrant activation of PI3K-Akt pathway may contribute to increased cell invasiveness and facilitate prostate cancer progression.
- mTOR regulates the phosphorylation and activation of Akt in endothelial cells and a major effect of mTOR inhibition in endothelial cells is to suppress Akt-inducible pro-survival signals
- P-Rex1 links mTOR signaling to Rac activation and cell migration
- LA's ability to inhibit apoptosis and proliferation of ECs could beneficially affect endothelial dysfunction, which precedes manifestation of late diabetic vascular complications.
- peripherin is a novel substrate for Akt in vivo and its phosphorylation may play a role in motor nerve regeneration
- Akt/PKB interacts with the histone H3 methyltransferase SETDB1 and coordinates to silence gene expression.
- analysis of calcium/calmodulin binding to the pleckstrin homology domain of AKT1
- IGF-I and insulin promoted the growth of human acute myeloid leukemia blasts in vitro and activated the phosphoinositide 3-kinase (PI3K)/Akt and the extracellular signal-regulated kinase (Erk) pathways
- Chromogranin A can increase prostatic cancer cell survival through AKT up-regulatoin.
- CD44-induced cell migration is dependent on its complex formation with Lyn and its consequent regulation of AKT phosphorylation in colon cancer cells.
- The inhibition of Akt and S6K1 phosphorylation by PRR5 knock down correlates with reduction in the expression level of platelet-derived growth factor receptor beta (PDGFRbeta).
- These results demonstrate that "pure" isoprenoids and genistein differentially impact cap-dependent translation in tumor cell lines.
- loss of PTEN expression, together with increased Akt phosphorylation, contributes to progression and recurrence of prostate cancer
- activation of the PI3K-Akt pathway during liver oncogenesis may be at least partially responsible for the elimination of HBV replication from tumor cells
- E17K mutation activates AKT1 by means of pathological localization to the plasma membrane, stimulates downstream signalling, transforms cells and induces leukaemia in mice; this mechanism indicates a direct role of AKT1 in human cancer
- In the absence of EGF, p38MAPK-activated AKT is necessary for HER-2 overexpressing human breast cancer cells to survive and to form colonies in soft agar.
- CTMP induces translocation of Akt to the membrane and thereby increases the level of Akt phosphorylation. As a result, CTMP enhances various cellular activities that are principally mediated by the PI3-kinase/Akt pathway.
- a subpopulation of Akt is cholesterol sensitive and the oncogenic effects conferred by myristoylation arise, in part, from the tendency of the membrane-targeted form of the protein to reside in cholesterol-rich membrane microdomains
- IKK alpha controls mTOR kinase activity in Akt-active, PTEN-null prostate cancer cells, with less involvement by IKK beta
- AKT amplification and the mTOR/p70S6K1 pathway play an important role in human lung cancer cells acquiring CDDP resistance
- Phosphoinositide 3-kinase-independent non-genomic signals transit from the androgen receptor to Akt1 in membrane raft microdomains
- BCR/ABL-Y177 plays an essential role in Ras and Akt activation and in human hematopoietic progenitor transformation in chronic myelogenous leukemia
- NGF stimulates endothelial cell invasion and cord formation by augmenting MMP-2 via the PI3K/Akt signaling pathway and AP-2 transcription factor, which may be responsible for triggering angiogenesis.
- PTEN dominantly inhibits Akt activation, the coexistence of high levels of the PTEN protein with enhanced Akt activation suggests the existence of novel mechanisms which attenuate PTEN
- Expression analysis of additional genes, AKT1, NOG and its antagonist BMP4, which interact downstream to FGFR1, demonstrated expression differences between primary rhabdomyosarcoma tumors and normal skeletal muscles
- activation of PRPK is mediated by another kinase, Akt/PKB, which phosphorylates PRPK at Ser250
- These results suggested that PKB enhanced DNMT1 stability and maintained DNA methylation and chromatin structure, which might contribute to cancer cell growth.
- Overexpression of Akt1 upregulates glycogen synthase activity and phosphorylation of mTOR in IRS-1 knockdown HepG2 cells.(
- Activation of AKT, possibly through the PI3K-AKT pathway, is an important component of ASCC tumorigenesis that contributes to MDM2 and TP53 accumulation in the nucleus.
- The role of P-AKT in multidrug resistance of gastric cancer cells and the possible underlying mechanisms are here investigated
- Akt blocks MstI-triggered FOXO3 nuclear translocation by phosphorylating MstI, promoting cell survival.
- down-regulation of Akt induced cytotoxicity of WM cells in the bone marrow microenvironment and inhibited migration and adhesion in vitro.
- Concluded that Wnt5a is a natural ligand of Fzd3 that triggers the PI3K/Akt signal and promotes adhesion of human dermal fibroblasts.
- Cutaneous human papillomaviruses down-regulate AKT1.
- Activation of PKB is associated with astrocytic tumor pathogenesis and progression
- Use of resveratrol or inhibition of Akt phosphorylation may represent an important therapeutic approach in combination with conventional therapies for the treatment of prostate cancer.
- We found significantly decreased RNA levels in prefrontal cortex of schizophrenic individuals, consistent with reduced AKT1 protein levels reported in schizophrenic brain.
- the AKT1 PH domain and hinge region as functional domains which jointly permit AKT1 translocation and phosphorylation in response to extracellular pressure
- Inhibition of PI3K signaling by PTEN inhibits tumor angiogenesis and growth. AKT is the downstream target of PI3K in controlling angiogenesis and tumor growth.
- IGF-1 activates the IGF receptor/IRS/PI3K/PKB pathway, and that PI3Kalpha is essential for the potentiatory effect of IGF-1 on platelet responses
- plexin-B1 promotes endothelial cell motility through RhoA and ROK by regulating the integrin-dependent signaling networks that result in the activation of PI3K and Akt
- Akt inhibition primes TRAIL-resistant cells to TRAIL-induced apoptosis.
- Platelet PAR-1/PAR-4 stimulation causes rapid Akt phosphorylation downstream of PLC, whereas with continuous stimulation, ADP and PI3K are required for maintaining Akt phosphorylation.
- important novel role for PKB in regulation of cell fate choices during hematopoietic lineage commitment
- Triple-negative breast cancers are characterized by increased phosphorylation of Akt kinase
- PKB[alpha] and/or PKB[gamma] and not PKB[beta] alone are involved in gemcitabine resistance mechanisms.
- Constitutive Akt activation is required for EGF to prevent neuroendocrine differentiation of prostate cancer cells.
- VEGF regulates angiopoietin-Tie2 signaling by inducing proteolytic cleavage and shedding of Tie2 via a novel PI3K/Akt-dependent pathway.
- Enhanced angiotensin converting enzyme 2 regulates the insulin/Akt signalling pathway by blockade of macrophage migration inhibitory factor expression.
- findings suggest that cigarette smoking is associated with the formation of LDL subfraction L5, which inhibits endothelial progenitor cell differentiation by impairing Akt phosphorylation via the LOX-1 receptor
- Akt1 and Akt2 mediate GPIb-IX signaling via the cGMP-dependent signaling pathway.
- HER-2/neu transcriptionally activates Jab1 expression via the AKT/beta-catenin pathway in breast cancer cells.
- AKT1 is a susceptibility gene for schizophrenia in the Chinese population and may play no major role in the therapeutic response to antipsychotics or in chlorpromazine-induced extrapyramidal syndrome.
- A novel point mutation (E17K) in the pleckstrin homology domain (PHD) of the AKT1 gene in human cancers was discussed.
- High levels of p-AKT expression occurred independently of the presence of PTEN or PIK3CA mutations in endometrial cancer.
- pleiotrophin potentiates cardiomyocyte cell death, at least partially, through inhibition of AKT signaling
- Akt and Mcl-1 are major components of a survival pathway that can be activated in CLL B cells by antigen stimulation.
- Mst1 and its caspase cleavage products are direct inhibitors of Akt
- p53 is an indispensable component of cellular signaling system which is regulated by caveolin-1 expression, involving Akt activation and increase in cyclin D1, thereby promoting proliferation of breast cancer cells.
- hypoxia could inhibit the SDF-1-dependent migration of HL-60 via blocking of Akt activation.
- modulation of phosphatidylinositol 3-kinase/Akt/GSK3beta signaling cascades can be beneficial for protecting or facilitating recovery from cellular LeTx intoxication in cells that depend on basal MEK1 activity for proliferation.
- Akt1 is a crucial regulator of osteoblasts and osteoclasts by promoting their differentiation and survival to maintain bone mass and turnover
- Parainfluenza virus 5 V protein interacts with Akt, a serine/threonine kinase, also known as protein kinase B.
- BCL2 functions as an activator of the AKT signaling pathway in pancreatic cancer.
- the ability of NF-kappaB to regulate the G1-phase expression of key proto-oncogenes is subject to regulation by the integrated activity of IkappaB kinase (IKK)alpha, IKKbeta, Akt and Chk1
- Impaired insulin signaling through Akt and AS160 in part explains insulin resistance at the molecular level in skeletal muscle in polycystic ovary syndrome.
- PI3-K/Akt pathways have a dual role in both survival and cell death processes depending on the stimulus.
- results indicate that shRNA targeting of tNOX inhibits the growth of cervical cancer cells, and reduces cell migration via a decrease in the membrane association of Rac.
- Our data suggest a crucial role of Ki-Ras:Akt1 complex in NF-kappaB transcriptional activation and enhancement of cell survival.
- Pim-1 is a crucial facet of cardioprotection downstream of Akt
- Levels of phospho-Akt are decreased in Caki cells overexpressing Par-4. inactivation of Akt is important in cellular pathways affected by Par-4.
- AKT1 inhibitors counteract the bacterial manipulation of host signalling processes, thus controlling intracellular growth of bacteria
- a key regulatory role of the Akt/mTOR pathway in the generation of the effects of As(2)O(3)
- The results from this investigation show that GBS both requires and activates the PI3K/Akt host-cell signalling pathway during invasion of epithelial cells.
- No mutations in AKT1 pleckstrin homology domain were identified, making this mutation an unlikely cause of PI3K/AKT pathway activation in acute myeloid leukaemia
- betaenin can be involved in polyphenol mediated down regulation of AKT1.
- Chorionic gonadotropin promotes trophoblast invasion and migration through activation of ERK and AKT signaling involving their downstream effector MMP-2.
- These data provide the first evidence that IL-18 and FN stimulate each other's expression
- Altogether these results highlight an intertwined role for specific Akt isoforms and XIAP in chemoresistance of uterine cancer cells.
- Signal transduction pathways underlying the enhanced cell migration reveal that the IGF-I-IGFBP-VN complex stimulates a transient activation of the ERK/MAPK signaling pathway and a sustained activation of the phosphatidylinositide 3-kinase/AKT pathway.
- The activation of the protein kinase B (Akt) signaling cascade by carbon nanoparticles was investigated with regard to its relevance for proliferation.
- support the role of Notch and Akt in breast cancer progression
- CD28 costimulation activates AKT to phosphorylate NF90 at Ser647 and phosphorylation triggers NF90 to relocate to the cytoplasm and stabilize IL-2 mRNA.
- Hsp27 inhibits oxidative stress-induced H9c2 damage and inhibition of ROS generation and the augmentation of Akt activation may be involved in the protective signaling.
- in most primary brain tumors, AKT is activated by molecular mechanisms other than oncogenic G49A mutations of AKT1
- RIG1 plays a role in IFN-gamma-mediated therapy by downregulating p185 and its downstream PI3K/Akt/mTOR/VEGF-signaling pathway
- These results suggest that 0.05 Gy of ionizing radiation stimulates cell proliferation through the transient activation of Raf and Akt in CCD-18 Lu cells.
- The overexpression may be a powerful prognostic marker for predicting disease free and overall survival of breast cancer patients.
- Rac signaling to cyclin D1 is a crucial pro-proliferative effect of E-cadherin-mediated cell-cell adhesion
- Treatment of cells with arsenite also induced significant activation of PI-3K and Akt, which was responsible for the anchorage-independent cell growth induced by arsenite exposure.
- t-Darpp promotes cancer cell survival by up-regulation of Bcl2 through Akt-dependent mechanism.
- miR-214 induces cell survival and cisplatin resistance primarily through targeting the PTEN/Akt pathway.
- These results suggest that caffeine has a cytoprotective effect due to the activation of the PI3K/Akt pathways in SH-SY5Y cells.
- The subcellular localization of DNMT1 can be altered by the addition of IL-6, and this process is greatly enhanced by phosphorylation of the DNMT1 nuclear localization signal (NLS) by PKB/AKT.
- The phosphorylation pattern and kinase activity of each Akt isoform were compared in primary myotubes from healthy control participants and type 2 diabetic patients.
- Poliovirus simultaneously activates the phosphatidylinositol 3-kinase (PI3K)/Akt survival signaling pathway in these cells, limiting the extent of JNK activation and thereby cell death.
- These findings revealed that TNF-alpha induced VCAM-1 expression via multiple signaling pathways.
- Human sarcopenia reveals an increase in SOCS-3 and myostatin and a reduced efficiency of Akt phosphorylation.
- the activities of AMP-activated protein kinase, protein kinase B, and mammalian target of rapamycin by limiting energy availability with 2-deoxyglucose
- Conclude that PI(3,4,5)P3 and PI(3,4)P2 have distinct roles in determining PKB phosphorylation and activity.
- These data provide evidence that, although AKT1 mutations are apparently rare in lung cancer (1.9%), the oncogenic properties of E17K-AKT1 may contribute to the development of a fraction of lung carcinoma with squamous histotype (5.5%).
- The results suggest that CKIepsilon is a new positive regulator of the Akt pathway. Here we propose that, rather than inhibiting PTEN function, CKIepsilon positively regulates Akt possibly by inhibiting Protein Phosphatase 2A (PP2A).
- the Akt/Girdin signalling pathway is essential in VEGF-mediated postneonatal angiogenesis
- the alpha6beta4 integrin strongly influence Akt phosphorylation through ErbB-3 protein regulation
- TNF-alpha overrides the G2/M checkpoint in keratinocytes and allows for some cells containing unrepaired cyclobutane pyrimidine dimers to enter the cell cycle. TNF-alpha seems to be dependent on PI3K-Akt activation.
- The effect of IL-2 on angiogenesis and tube formation was mediated by Reactive Oxygen Species and Akt.
- Girdin has an important role in tumor progression with aberrant activation of the Akt signaling pathway
- PKC epsilon mediates TRAIL resistance by Akt-mediated phosphorylation of Hdm2 resulting in suppression of p53 expression and downregulation of Bid in breast cancer cells
- These findings indicate that v-Crk controls cell migration and membrane dynamics by activating Rac in CAS-deficient mouse embryo fibroblasts.
- In dermal fibroblasts, Akt has dual profibrotic effects, increasing collagen synthesis and decreasing degradation by MMP1 downregulation. Systemic sclerosis fibroblasts were more sensitive to Akt inhibition, with respect to collagen and MMP1 production.
- the activities of specific elements of the PI3K signaling pathway, including Akt, are necessary for the synergistic induction of MMP-1 and MMP-13 and the cartilage breakdown stimulated by IL-1 and oncostatin M
- isosilybin B treatment enhances the formation of complex between Akt, Mdm2 and AR, which promotes phosphorylation-dependent AR ubiquitination and its degradation by proteasome
- VprBP depletion abolished the in vivo interaction of Merlin and Roc1-Cullin4A-DDB1, which resulted in Merlin stabilization and inhibited ERK and Rac activation
- Akt and mTOR activation have distinct functional relevance in mantle cell lymphoma
- Active AKT and mTOR, were present in all adenomas, carcinomas, and in normal colorectal mucosa.
- cAMP inhibits cell migration by interfering with Rac-induced lamellipodium formation
- The Akt isoforms are required for the HGF-stimulated invasive growth of human salivary gland cancer cells.
- post-translational modification by nitrotyrosylation does not control Akt in systemic sclerosis platelets
- stabilization of MDMX by Akt may be an alternative mechanism by which Akt up-regulates MDM2 protein levels and exerts its oncogenic effects on p53 in tumor cells
- Results identify a molecular mechanism by which activated FGFR2 recruits Cbl in raft micro-domains to trigger PI3K ubiquitination and proteasome degradation, and reveal a role for PI3K/Akt in the control of osteoblast survival by FGFR2 signaling.
- Despite the confirmed oncogenic function of the AKT1 E17K, the rare incidences of the mutation suggest that it may not play a crucial role in the development of the most common types of human cancers.
- The PI3K/Akt/mTOR signaling pathway is implicated in the development of cervical cancer.
- The data presented here suggest the involvement of AKT1 in protection of PD through many possible mechanisms involving different signaling pathways that could be potential therapeutic targets in the future.
- Bortezomib -sensitive and -resistant MCL cell lines showed comparable activation of the AKT pathway
- Our data indicate a novel role for Akt in supporting the progression of human melanomas
- chlorophyllin exerts antioxidant effect by inducing HO-1 and NQO1 expression mediated by PI3K/Akt and Nrf2
- Prognostic and/or predictive role of Akt phosphorylation in breast, prostate and non-small cell lung cancer. Review.
- AKT1 pleckstrin homology domain (E17K) mutations do not play a roles in chronic lymphocytic leukaemia and acute myeloid leukaemia
- the TSC1-TSC2 complex inhibits mTORC1 and activates mTORC2, which through different mechanisms promotes Akt activation
- AKT is activated in an ataxia telangiectasia and Rad3-related-dependent manner in response to temozolomide and confers protection against drug-induced cell growth inhibition.
- in VSMCs exposed to hyperglycemia, IGF-I stimulation of Shc facilitates the transfer of Grb2 to p85 resulting in enhanced PI3K activation and AKT phosphorylation leading to enhanced cell proliferation and migration
- activation of Akt during preoperative chemotherapy for esophageal cancer correlates with poor prognosis
- Cav-1 increases the basal and TGF-beta1-induced expression of type I procollagen by regulating two opposite signaling pathways: inhibiting TGF-beta1/smad signaling and activating a PI-3 kinase/Akt/mTOR-dependent pathway in human dermal fibroblasts.
- tetrandrine induces G(1) arrest and apoptosis through PI3K/kip1/AKT/GSK3beta pathway
- Activin A may mediate ovarian oncogenesis by activating Akt and repressing GSK to stimulate cellular proliferation.
- This study provides a direct link between the growth factor signaling pathways regulated by PI3 kinase/Akt and MAP kinases with Myc-mediated transcription.
- Transforming growth factor beta induces apoptosis through repressing the phosphoinositide 3-kinase/AKT/survivin pathway in colon cancer cells.
- The interplay between cancer cell-derived clusterin and IGF-1 may dictate the outcome of cell growth and dormancy during tumorigenic progression.
- Akt and its downstream targets FoxO3a and GSK3 regulate a survival pathway in VSMCs and that their deregulation due to a reduction of IGF1R signaling may promote apoptosis in atherosclerosis.
- High NG2/MPG expression correlated with multidrug resistance mediated by increased activation of alpha3beta1 integrin/PI3K signaling and their downstream targets, promoting cell survival
- ADAM17 mediates the EGFR/AKT/cyclin D1 pathway and cell cycle progression to the S phase induced by UVA radiation
- deregulated PKB/AKT stabilizes Mcl-1 expression in a mammalian target of rapamycin (mTOR)-dependent pathway
- Although Akt activation leads to GSK-3beta phosphorylation and the subsequent expression of beta-catenin, activation of this pathway by 1-azakenpaullone was insufficient to stimulate the motile phenotype in cytotrophoblasts.
- Cdk5 phosphorylates PIKE-A and stimulates its GTPase activity, which activates nuclear Akt and promotes glioblastoma cell migration and invasion.
- results demonstrate that an insulin or TNF response that uses Akt-dependent signaling activates IKKalpha to induce mTOR activity, whereas a TNF response that does not involve Akt activates IKKbeta to activate mTOR
- 7-ketocholesterol-induced apoptosis has a role in phospholipidosis and down-regulation of the PI3-K/PDK-1/Akt signalling pathway
- AKT1 has a role in modulating human prefrontal-striatal structure and function and the mechanism of this effect may be coupled to dopaminergic signaling and relevant to the expression of psychosis
- GILZ is a mediator of glucocorticoid killing, and is regulated by PI3-kinase/AKT.
- A signaling cascade for the regulation of p53 in response to ionizing radiation was proposed that involves activation of DNA-PK and Akt/PKB and inactivation of GSK-3 and Mdm2.
- Shorter overall survival in primary melanoma was associated with the presence of ulceration and BRAF exon 15 mutations, as well as the absence of nuclear activation of Akt and of cytoplasmic activation of ERK.
- Osteoblast-derived BMP-2 act through Akt and ERK, which in turn activates IKK alpha/beta and NF-kappaB, resulting in the activations of beta1 and beta 3 integrins and contributing the migration of prostate cancer cells.
- The mTOR-associated protein Raptor is required for the ability of Akt to induce NF-kappaB activity.
- Akt inactivation in breast cancer causes negative regulation of INK4a/ARF-independent cell cycle progression by Mel-18
- LMP1 triggers the PI3K/Akt pathway to inactivate FOXO3a and decrease DDB1, which can lead to repression of DNA repair and may contribute to genomic instability in human epithelial cells
- The percentage of positive cells for TKTL1 and p-Akt was significantly correlated in glioblastoma multiforme (GBM) and other astrocytic gliomas (AGs, grades II and III).
- strongly activated in HTLV-1 infected T cell lines derived from HAM/TSP patients.
- Nuclear Akt phosphorylates Aly on threonine-219, which is required for its interaction with Akt.
- hnRNP A1 has a role in mediating rapamycin-induced alterations of cyclin D1 and c-myc IRES activity in an Akt-dependent manner and provide the first direct link between Akt and the regulation of IRES activity
- These results indicate that FSH increases the expression of VEGF by upregulating the expression of survivin, which is activated by the PI3K/AKT signaling pathway.
- Alterations to the Akt signaling pathway and nuclear export determine the stability of AIB1 and nuclear content of this coactivator.
- HDL has endothelial barrier promoting activities, which are attributable to its S1P component and signaling through the S1P1/Akt pathway.
- CCL2 protects prostate cancer PC3 cells from autophagic death via the phosphatidylinositol 3-kinase/Akt/survivin pathway
- Akt and AMPK have roles in the pathway of hydrogen peroxide-activated endothelial nitric-oxide synthase phosphorylation and function
- Akt-mediated phosphorylation modulates eNOS uncoupling and greatly increases O(2)* generation from the enzyme at low Ca(2+) concentrations, and PKCalpha-mediated phosphorylation alters the sensitivity of the enzyme to other negative regulatory signals.
- Datas show that transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to trastuzumab.
- analysis of Akt-dependent and Akt-independent multiple myeloma subgroups
- Authors observed a significant increase in AKT phosphorylation in depressed ventral tegmental area postmortem samples from depressed patients, without a change in total AKT levels.
- the PI3K/Akt pathway is involved in MDR in lymphoma cell lines and PI3K/Akt inhibition correlates down-regulation of NF-kappaB activity and inhibition Pgp function.
- The effect of AKT1 on DNA-dependent protein kinase catalytic subunit (DNA-PKcs) activity and DNA-dsb repair in irradiated non-small cell lung cancer cell lines A549 and H460, was analysed.
- eIF4E knockdown is not associated with Akt activation.
- The lack of Par-4 dramatically enhances Ras-induced lung carcinoma formation in vivo, acting as a negative regulator of Akt activation.
- results show that the mutation E17K/AKT1 was not detected in the pleckstrin homology domain of AKT1 of the investigated cases. We conclude that this mutation is not a major event in B-cell-derived lymphoid leukaemias
- endocrine hormone insulin contributes to VEGF release in skin wounds through an Akt1-and 4E-BP1- mediated posttranscriptional mechanism in keratinocytes
- Data demonstrate need for autophagy-mediated degradation of toxic, mutated arginine vasopressin C98X peptides, and suggest that, in the presence of mis-folded proteins, the stimulation of Akt signalling counteracts autophagy and precipitates cell death.
- PIK3CA mutations, in comparison with PTEN loss and AKT1 mutations, were associated with significantly less and inconsistent activation of AKT and of downstream PI3K/AKT signaling in tumors and cell lines
- PAK1-specific paxillin phosphorylation at Ser(273) is critically involved in the positive-feedback regulation of the Rac-PAK1 pathway.
- The role of PI3K/Akt activity and DNA-PKcs on XRCC1 expression/stabilization, was studied.
- FASN and activated AKT pathway may be a potential target for therapeutic intervention for the treatment of papillary thyroid carcinomas.
- results suggest that both Transketolase-like enzyme 1 (TKTL1) and p-Akt protein play an important role in the progression of cervical neoplasia
- isoflavone-induced inhibition of cell proliferation and induction of apoptosis are partly mediated through the regulation of the Akt/FOXO3a/GSK-3beta/AR signaling network.
- Tissue kallikrein decreased GSK-3beta activity via the phosphatidylinositol 3-kinase-Akt pathway and enhanced VEGF and VEGFR-2 expression in endothelial cells.
- analysis of differential Akt regulation in plasma membrane microdomains
- endosomal activation of the PI3K/AKT signaling pathway in response to Gbetagamma trafficking, via its interaction with Rab11, is a relevant step in the mechanism controlling cell survival and proliferation
- Peroxisome proliferator-activated receptor-delta agonist enhances vasculogenesis by regulating endothelial progenitor cells through genomic and nongenomic activations of the phosphatidylinositol 3-kinase/Akt pathway
- DIDS-sensitive Cl- channels play a key role in the Low-density lipoprotein-induced cell proliferation of human aortic smooth muscle cells via the activation of Erk1/2 and PI3K/Akt and the upregulation of Egr-1.
- data demonstrate a unique role for Akt in inhibiting TR3 functions that are not related to transcriptional activity but that correlate with the regulation of its mitochondrial association
- in breast DCIS patients, strong cytoplasmic and/or nuclear immunoexpression was revealed in 17 cases for NRGalpha, 13 cases for p-AKT, and nuclear immunoexpression with p-MAPK was found in 17 cases.
- Fstl1 is a secreted muscle protein or myokine that can function to promote endothelial cell function and stimulates revascularization in response to ischemic insult through its ability to activate Akt-eNOS signaling
- These results suggest that the BMP-2 acts through PI3K/Akt, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of beta1 integrin and contributing the migration of human chondrosarcoma cells.
- These results reveal a primary role of Akt in shaping intracellular Ca2+ homeostasis, that may underlie its protective role against some proapoptotic stimuli.
- Direct inhibition of Akt may represent a therapeutic strategy for breast and other cancers.
- rac regulates its effector phospholipase Cgamma2 through interaction with a split pleckstrin homology domain
- Gate control for cell polarization can explain how Rac can be employed for both PI3K-dependent and -independent signaling pathways coexisting in the same cell.
- no aberrant SSCP pattern in exon 2 of the AKT1 gene was found, indicating that there were no E17K mutations of the AKT1 gene in these samples of gastrointestinal and liver cancers in the Korean patients
- anti-apoptotic functions of cFLIPs may be attributed to inhibit oxaliplatin-induced apoptosis through the sustained XIAP protein level and Akt activation.
- These findings demonstrate that HAPO induces endothelial cell proliferation through the PI-3K/Akt pathway.
- Inhibition of PI3-K/Akt induces a 40% decrease of cyclin D1 half-life as a result of accumulation of the dephosphorylated/active form of GSK-3beta within the nucleus, where it can phosphorylate cyclin D1 on Thr286 thereby promoting its nuclear export.
- Confocal imaging of fluorescently labeled ZEBOV indicated that inhibition of PI3K, Akt, or Rac1 disrupted normal uptake of virus particles into cells and resulted in aberrant accumulation of virus into a cytosolic compartment
- Glycine-extended gastrin induced signalling involves a JAK2/PI3-kinase/Akt/NF-kappaB sequence leading to COX-2 transcription.
- there are two parallel cell-survival pathways in prostate cancer cells: a strong Akt-independent, but rapamycin-sensitive pathway downstream of mTORC1, and an AR-dependent pathway downstream of mTORC2 and Akt, that is stimulated by mTORC1 inhibition
- These findings demonstrate that PI3K/Akt signaling is a key regulator in terminal chondrocyte differentiation in both embryonic and adult chondrogenesis.
- H. pylori infection of gastric epithelial cells induced phosphorylation of Akt at Ser 473 and Thr 308.
- AKT1 (E17K) G-->A mutation was not detected in any of the pancreatic cancer tissue samples nor in any cell line DNA; results indicate that the AKT1 (E17K) mutation may not play a significant role in pancreatic cancer
- COX-2 promotes colon tumor progression, but not initiation, and it does so, in part, by activating EGFR and Akt signaling pathways
- Suppression of LKB1 expression led to apoptosis in three cell lines in which Akt is constitutively active but not in two cell lines without Akt activation.
- PTH induction of apoptosis is mediated by translocation of mitochondria to the perinuclear region, dephosphorylation of Akt, dephosphorylation of Bad and its movement to the mitochondria, release of cytochrome c and Smac/Diablo, activating casp3.
- an activating mutation of AKT1 found in prostate cancer
- activation of the Akt-mTOR-p70S6K pathway plays a significant role in HCC progression by promoting neoangiogenesis.
- Activated Akt seems to characterize well-differentiated invasive squamous laryngeal carcinomas, loss of E-cadherin and activation of beta-catenin correlated with high grade carcinomas.
- HuR is a direct transcription target of NF-kappaB; its activation in gastric cancer cell lines depends on phosphatidylinositol 3-kinase/AKT signaling. HuR activation by this pathway has proliferative and antiapoptotic effects on gastric cancer cells.
- AKT was expressed in 83.3% of ameloblastomas, showing high expression of the p-thr(308)AKT and p-ser(473) AKT forms in 93.3% and 56.6% of cases, respectively.
- nuclear factor kappaB is inhibited through an AKT-independent pathway by liposome-encapsulated curcumin suppresses growth of head and neck squamous cell carcinoma in vitro and in xenografts
- Complement C1q chemoattracts human dendritic cells and enhances migration of mature dendritic cells to CCL19 via activation of AKT and MAPK pathways.(
- These results suggest a unique role of AKT in modulating estrogen signaling in ERalpha-positive breast cancers and highlights how extracellular signal activated kinases can change the landscape of transcription factor binding to the genome.
- there was a significant inverse correlation between nuclear pAkt and apoptotic index and between cytoplasmatic and nuclear pAkt and patient survival.
- These data demonstrate that integrin/EGFR cross-talk is required for expression of Egr-1 through a novel regulatory cascade involving the activation of the PI3K/Akt/Forkhead pathway.
- SEMA3B is a potential tumor suppressor that induces apoptosis in SEMA3B-inactivated tumor cells through the Np-1 receptor by inactivating the Akt signaling pathway.
- the Akt signalling pathway is inhibited by NO-sulindac, which inhibits the hypoxia response of PC-3 prostate cancer cells
- DEP-1 is a positive regulator of VEGF-mediated Src and Akt activation and endothelial cell survival.
- PTEN upregulation is responsible for Pfn1-dependent attenuation of AKT activation in MDA-MB-231 cells.
- These data indicate that skeletal muscle is a source of FGF21 and that its expression is regulated by a phosphatidylinosistol 3-kinase (PI3-kinase)/Akt1 signaling pathway-dependent mechanism.
- Following down-regulation of MR-1, the phosphorylations of MLC2, focal adhesion kinase (FAK), and Akt were dramatically decreased
- HMGB1 induced the activation of p38MAPK, ERK1/2 and Akt.
- In vitro studies reveal that the E17K mutation of ATK1 PH domain dramatically increases the affinity for the constitutive plasma membrane lipid PI(4,5)P(2)
- In human melanoma cells, MFG-E8 knockdown attenuated Akt and Twist signaling and thereby compromised tumor cell survival, EMT, and invasive ability
- these results indicate the importance of C. burnetii modulation of host signaling and demonstrate a critical role for Akt and Erk1/2 in successful intracellular parasitism and maintenance of host cell viability.
- Scleroderma serum-induced EPC apoptosis is mediated chiefly by the Akt-FOXO3a-Bim pathway, which may account, at least in part, for the decreased circulating EPC levels in scleroderma patients.
- VacA activates the PI3K/Akt signaling pathway, resulting in phosphorylation and inhibition of GSK3beta, and subsequent translocation ofbeta-catenin to the nucleus, consistent with effects of VacA on beta-catenin-regulated transcriptional activity.
- Results indicated that the JNK and Akt pathways and inhibition of NF-kappaB activity were key regulators of apoptosis in response to withaferin A in human leukemia U937 cells.
- AKT1 inhibits homologous recombination by inducing cytoplasmic retention of BRCA1 and RAD51.
- Altered insulin activation of the PI3K/Akt but not the MAPK pathway precedes and may contribute to development of whole-body insulin resistance and type 2 diabetes in men with low birth weight.
- NGF induces Mac-2BP expression via the PI3K/Akt/NF-kappaB pathway.
- RGS13 overexpression inhibited CXCL12-evoked Ca(2+) mobilization, Akt phosphorylation and chemotaxis.
- mTORC2 and Akt facilitate CD40-inducible expression of VEGF in endothelial cells
- ILK overexpression during liver oncogenesis and cirrhosis correlates with activation of Akt but not with other conventional ILK targets
- glioma cells enhance EPC angiogenesis via VEGFR-2, not VEGFR-1, mediated by the MMP-9, Akt and ERK signal pathways
- The association and altered regulation of IRS proteins by Ad5E1A contribute to the adenovirus-transformed phenotype and modulates viral infection in an Akt-dependent manner.
- ZAP70 expression levels in B cells give an estimate of the proliferative potential and the associated protein kinase B availability.
- Akt signals are involved in decoy receptor 3 expression in PANC-1 human pancreatic epithelioid carcinoma cells.
- These data demonstrated that cell adhesion-mediated PI3K/Akt activation could be one of the important mechanisms of resistance to genotoxin-induced cell death in differentiated epithelial cells.
- Overexpression of P-AKT and NF-kappaB p65 were involved in the carcinogenesis and metastasis of ovarian cancer.
- results suggest that CCL5 acts through PI3K/Akt, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activation of alphavbeta3 integrin and contributing to the migration of human lung cancer cells
- the c-Src-Rac1-p38 MAPK pathway is required for activation of Akt in response to radiation and plays a cytoprotective role against radiation in human cancer cells
- Promoter hypermethylation of CST6 is associated with aberrant AKT1 activation in epithelial cells, as well as the disabled INNP4B regulator resulting from the suppression by cancer associated fibroblasts.
- the pathway of apoptin-induced apoptosis and show that it essentially depends on abnormal phosphatidylinositol 3-kinase (PI3-kinase)/Akt activation, resulting in the activation of the cyclin-dependent kinase CDK2
- KAI1/CD82 decreased the metastatic phenotype of H1299 lung carcinoma cells by down-regulating Rac1 expression through the PI3K/Akt/mTOR pathway.
- These results suggest the anti-inflammatory activity of platonin is a result of reduced NF-kappaB activity due to inhibition of Akt and IKKbeta.
- Akt may induce anti-apoptotic signals at least in part through the regulation of the amount and activity of Bcl-w.
- the PTEN/PI3K/Akt pathways are critical for prostate cancer stem-like cell maintenance
- ligation of ApoER2 by APC signals via Dab1 phosphorylation and subsequent activation of PI3K and Akt and inactivation of GSK3beta, thereby contributing to APC's beneficial effects on cells.
- pneumococci exploit the vitronectin-alphavbeta3-integrin complex as a cellular receptor for invasion and this integrin-mediated internalization requires the cooperation between the host signalling molecules ILK, PI3K and Akt.
- AKT1 pleckstrin homology domain mutation appear to be rare in Japanese gastrointestinal and liver cancer patients.
- Trends suggested down-modulation of cyclooxygenase-2 and Ki-67 in some tissues, increased pAKT-Ser473 expression, and an inverse relationship between PGE(2) and BCL2 expression.
- AKT activation has a role in hypoxia-increased prostate epithelial cell resistance to receptor-mediated apoptosis
- EGFR signals to mTOR through PKC and independently of Akt in glioma
- Study identifies PHLDA3 as a p53 target gene that encodes a PH domain-only protein and finds that PHLDA3 competes with the PH domain of Akt for binding of membrane lipids, inhibiting Akt translocation to the cellular membrane and activation.