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Validated All-in-One™ qPCR Primer for STAT1(NM_007315.3) Search again
Product ID:
HQP017764
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CANDF7, IMD31A, IMD31B, IMD31C, ISGF-3, STAT91
Gene Description:
signal transducer and activator of transcription 1
Target Gene Accession:
NM_007315.3(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
The protein encoded by this gene is a member of the STAT protein family. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. This protein can be activated by various ligands including interferon-alpha, interferon-gamma, EGF, PDGF and IL6. This protein mediates the expression of a variety of genes, which is thought to be important for cell viability in response to different cell stimuli and pathogens. Two alternatively spliced transcript variants encoding distinct isoforms have been described. [provided by RefSeq].
Gene References into function
- soluble factor(s) secreted from CD8(+) T lymphocytes inhibits human immunodeficiency virus type 1 replication through STAT1 activation
- We conclude that STAT1 activation is necessary but not sufficient for induction of transcription of IFN gamma-responsive genes
- IFNtau effect on IRF-1 expression is primarily regulated by tyrosine-phosphorylated Stat1alpha or Stat1beta dimers
- Cytokine signaling: STATS in plasma membrane rafts
- STAT1 plays a minimal role in TNF-mediated cellular responses
- phosphorylation on serine 727 by protein kinase C-delta
- Stat1 and Stat3 may support cell growth in part via c-myc gene activation in primary erythroleukemia cells.
- identification as a molecular target of IGFBP-3 during chondrogenesis
- Isolation and characterization of a human STAT1 gene regulatory element. Inducibility by interferon (IFN) types I and II and role of IFN regulatory factor-1.
- Stat1-vitamin D receptor interactions antagonize 1,25-dihydroxyvitamin D transcriptional activity and enhance stat1-mediated transcription.
- results constitute genetic and biochemical evidence supporting a paramyxovirus-induced, IFN-independent STAT protein degradation complex that contains at least STAT1 and STAT2
- Requirement of Ca2+ and CaMKII for Stat1 Ser-727 phosphorylation in response to IFN-gamma
- Block of Stat-1 activation in macrophages phagocytosing bacteria causes reduced transcription of CIITA and consequent impaired antigen presentation.
- arginine/lysine-rich nuclear localization signals mediate interactions between dimeric STATs and importin alpha 5
- Distinct functions for STAT1 and PU.1 in transcriptional activation of Fc gamma receptor I promoter.
- Excessive P-Tyr-STAT1 responses could induce inflammatory cytokines and demyelination in MS, as in motheaten mice, which have defects in SHP-1 function. Abnormal interferon signaling may predict the course of MS and responses to therapy.
- Lipid microdomains are required sites for the phosphorylation and nuclear translocation of STAT1alpha.
- STAT1 phosphorylation of TcPTP is regulated by arginine methylation
- STAT-1, IRF-1, and RAR-beta expression were enhanced by IFN-gamma and ATRA in combination, and to a greater degree in BALM-3 cells than in BALM-1 cells, suggesting that these IFN-gamma related genes were involved in the induction of apoptosis.
- requirement in interferon-gamma-mediated inhibition in human chondrocytes
- STAT-dependent trans-activation is regulated by p38 MAPK and interferon gamma independent of serine phosphorylation
- Cells lacking STAT-1 show reduced apoptosis in response to heat or ischaemia. Expression of STAT-1 in these cells does not enhance cell death but restores sensitivity to stress-induced death.
- Stat1 phosphorylation is inhibited by SHP-2 and Stat1-dependent induction of luciferase activity is suppressed by SHP-2
- Nipah virus V protein evades alpha and gamma interferons by preventing STAT1 activation and nuclear accumulation
- Data suggest that down-regulation of interferon-gamma-mediated nuclear STAT1 binding in hepatocytes involves both dephosphorylation by mitogen-activated protein kinase phosphatase 1 and degradation by the ubiquitin-dependent proteasome pathway.
- Amino-termnal extensions of Sendai Virus C proteins induce pY701-Stat1 formation (while decreasing bulk Stat1 levels) in a manner that does not require interferon signaling
- We report two unrelated infants homozygous with respect to mutated STAT1 alleles. Both suffered from mycobacterial disease, but died of viral disease.
- Epstein-Barr virus SM protein induces STAT1 mRNA levels
- gp120 induces activation of STAT1, STAT3, and STAT5 in CD4+ cells of lymphocyte or monocyte/macrophage lineages.
- role for NFkappaB in LMP-1-mediated STAT1 expression in Epstein-Barr virus-immortalized cells
- results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase
- EGF-induced phosphorylation diminished the amount of this protein found in the clonal variants of A431 cells.
- Results provide evidence that interleukin-13 induces p38 MAP kinase phosphorylation and activation, which regulates Stat1 and Stat3 serine 727 phosphorylation.
- Data suggest that persistent STAT-1 activation can contribute to maintaining and expanding the local inflammatory response in Celiac Disease.
- Data suggest there is no defect in the JAK/STAT pathway in the tested melanoma cell lines, and that interferon resistance must be mediated through other components.
- a physical interaction between c-Fos and STAT-1 participates in NOS2 gene transcriptional activation in lung epithelium
- Measles virus V protein blocks INF-alpha/beta signaling by inhibiting STAT1 phosphorylation.
- STAT1-dependent transcription of pro-apoptotic and pro-inflammatory genes is regulated by IFN-gamma activated PI3K and mTOR pathways in a rapamycin-insensitive manner
- Stat1 and Stat3 exist as stable homodimers prior to activation
- STAT1 and STAT3 may, at least in part, mediate angiotensin II-induced TIMP-1 mRNA expression in human renal proximal tubular epithelial cells, implicating a role of the STAT signaling pathway in pathogenesis of renal tubulointerstitial fibrosis.
- STAT1 mediates differentiation of chronic lymphocytic leukemia cells in response to Bryostatin 1
- PIAS1 was found to strongly stimulate sumoylation of STAT1 at Lys703 by SUMO-1 conjugation to STAT1; results suggest a negative regulatory function for sumoylation.
- Interleukin-1 induces the phosphorylation of Stat1 on serine 727 but not on tyrosine 701
- HSP27-dependent thermotolerance is suppressed by mumps virus infection through the destruction of STAT-1.
- DNA-binding controls inactivation and nuclear accumulation of Stat1.
- potential mechanism for reduced NOS2 expression in cystic fibrosis is diminished signal transducer and activator of transcription-1 (STAT1) activity, possibly due to an increase in expression of protein inhibitor of activated STAT1 (PIAS1
- Differentiation-dependent expression of STAT1 may modify responses to growth factors in the cancers of the head and neck
- The results indicate that STAT1 activation play a crucial role in IFNalpha signaling for cytolysis function of NK cells.
- NF-kappaB, STAT1, and IRF-1 within HVSMCs could be central to a number of vascular pathologies and that inhibition of this pathway could be of therapeutic benefit.
- Hendra virus V protein inhibits cellular responses to IFN through binding and cytoplasmic sequestration of STAT1
- Sendai virus C protein prevents the gamma-activated factor from binding to gamma-activated sequence elements through its interaction with the STAT1 N-terminal domain.
- STAT1 tyrosine phosphorylation and DNA binding is dependent on Tc-PTP
- prolonged nuclear localization of activated STAT1 results in apoptosis involving specific regulation of caspase pathway
- On completion of fludarabine cycle 1, CLL cells showed increased STAT1 in the majority of patients, in contrast to the in vitro findings. This may reflect a survival advantage for cells that express high levels of STAT1
- ZBP-89 binds directly to the STAT1 promoter G-rich element
- there is progressive dysregulation of nuclear factor-kappa B and STAT1 in prostate cancer cells that leads to proangiogenic production of CXC chemokines.
- STAT1 has a role in IL-27 regulation of IL-12 responsiveness to naive CD4+ T cells
- interferon gamma Stat1 signaling in epithelial cells is disrupted by Helicobacter pylori infection
- IFN-gamma inhibits IFN-alpha-activated signals partly through the induction of STAT1 protein expression. Overexpression blocks IFNA-activated STAT2 translocation from IFNA receptor 2 to IFNA receptor 1, a critical step in IFNA signalling activation.
- Results demonstrate that induction of adenine nucleotide translocase 3 by interleukin-4 and interferon-gamma proceeds via pathways involving STAT6 and STAT1, respectively.
- Abnormally high amounts of Stat1, Stat5 and p21Cip1 proteins were found in prehypertrophic-hypertrophic chondrocytes, the extent of overexpression being directly related to the severity of the disease
- role of overexpression in tumors on radioresistance
- Epigenetic activation of the Jak/STAT pathway might have a tentative role in the pathogenesis of myeloma.
- the role of DNA binding in nuclear retention of Stat1; diminished N-domain-mediated oligomerization affected transcriptional activation by both Stat1 and Stat5a/b in a promoter-specific manner.
- the IGF-I receptor gene is a novel target for STAT1 action and that at least part of the inhibitory effects of STAT1 may involve repression of the strongly antiapoptotic IGF-I receptor gene
- STAT1 requires histone deacetylase activity for signaling
- expression of STAT-1 induced by Epstein-Barr virus (EBV) LMP-1 (latent membrane protein) and associated with EBV transformation and may be part of regulation of viral latency and cellular transformation
- Nuclear export by CRM1 created a nucleocytoplasmic Stat1 concentration gradient is significantly reduced by the blocking of energy-requiring translocation mechanisms
- STAT1 plays an important role in the regulation of erythropoiesis.
- imbalance between the antiproliferative/proapoptotic isoform STAT1alpha and the proliferative isoform STAT1beta is likely to play a crucial role in the regulation of proliferation and apoptosis
- IFN-alpha-induced nuclear accumulation of STAT1 was almost completely blocked in cell lines expressing high levels of HCV core protein.
- first 23 amino acids (C(1-23)) of the 204-amino-acid (aa)-long Sendai virus C protein act as an independent viral element that induce STAT1 degradation
- Protein kinase Cdelta regulates apoptosis via activation of STAT1.
- Coordinated Stat1 and NF-B activation, along with the lack of Stat3 activation, accounts for cytokine-stimulated GTPCH I induction in endothelial cells.
- STAT1 activation and interferon signaling blocked by West Nile Virus nonstructural proteins
- TPO and IFN-gamma activate the expression of TAP1 via a new mechanism that involves functional cooperation between STAT1 and IRF-2 on the TAP1 promoter
- These results imply that STAT-1 plays a crucial role in the DNA-damage-response by regulating the expression of 53BP1 and MDC1, factors known to be important for mediating ATM-dependent checkpoint pathways.
- LMP1-induced tyrosine phosphorylation of STAT1 is almost exclusively due to the NF-kappaB-dependent secretion of interferons in B cells. (stat1)
- HCV core protein binds STAT1, suggesting that this viral protein is associated with STAT1 degradation. STAT1 plays indispensable role in antiviral immunity against HCV expression. HCV subverts Jak-STAT kinase by selectively inducing STAT1 degradation.
- phosphorylation inhibited by human parainfluenza virus type 3 C protein.
- results demonstrate for the first time that prostacyclin receptor activation by cicaprost can lead to STAT1 and STAT3 phosphorylations via signaling pathways involving pertussis toxin-insensitive G proteins, ERK and JNK
- STAT1 and Nmi are downstream targets of Ets-1 in MCF-7 human breast cancer cells
- The hyperinsulinemia caused by this treatment may oppose the alterations in some gene expressions and the endothelial proliferation (cell growth-related gene expressions) that occur in established diabetes.
- Some antiapoptotic proteins were involved, but not STAT-1 alpha kinase, in resistance to TNF-alpha-dependent cell death promoting activity.
- IFNG priming enhances migration to inflammatory chemokines; IFN-gamma-inducible gene expression is attenuated by high levels of Stat1; physiological regulation of the relative abundance of Stat1 and Stat3 impacts on gene expression
- early vs late natures of the STAT1-dependent and STAT1-independent pathway responses in mice with primary DEN infection
- regulated nuclear export determines the cytokine sensitivity of the shuttling STAT1 transcription factors by controlling their availability at the receptor kinase complex
- STAT1, IRF1, and NF-kappaB activation and early myocyte apoptosis play a mechanistic role in septic myocardial depression and sepsis-induced organ dysfunction
- Rabies virus P protein does not induce STAT1 degradation and does not interfere with STAT1 phosphorylation. (Rabies virus P protein)
- results demonstrate that the conserved Leu-724 residue is a key residue that controls the maximal transcription activities of Stat1 in IFN-gamma signaling
- protein kinase Cdelta and JNK have roles in Ifn-alpha induced expression of phospholipid scramblase 1 through STAT1
- TNF-alpha and IFN-gamma regulate gene transcription mediated by NF-kappaB-Stat1 interactions
- over expression and purification of amino-terminal domain of STAT1; characterization by mass spectrometry and 2-dimensional nuclear magnetic resonance spectroscopy; results indicate that the N-terminus of hSTAT1 exists as a dimer in solution
- We conclude that the rate of activation of Stat1 in cells by IFN-gamma can be modified by regulating either receptor chain and speculate that pharmacological agents which modify receptor chain expression may alter IFN-gamma receptor signal transduction.
- The acetylation of Stat1 regulates NF-kappaB activity and thus ultimately apoptosis.
- Rabies virus P protein inhibits interferon signaling via activation-dependent binding to STAT1 and STAT2
- X-ray crystallographic analysis of human STAT1
- Intracellular HIV-1 Tat protein represses constitutive LMP2 transcription increasing proteasome activity by interfering with the binding of IRF-1 to STAT1
- changes in the relative expression and activation of STAT1 and STAT3 that occur during immune responses determine the nature of cellular responses to type I IFNs
- Effect of signal transducer and activator of transcription 1 proteins on indomethacin-induced cell division inhibition in chronic myelogenous leukemia cells.
- STAT-1alpha plays an important role in the atRA-induced transcriptional up-regulation of restin
- Data indicate that STAT1 plays a key role in the inhibition of angiogenesis through its action within vascular endothelial cells.
- The STAT1-SOCS1 pathway regulates the innate immune response via TLR3 signaling in epidermal keratinocytes.
- Neither the alleles, nor the genotypes in the case-control genetic association studies, nor the haplotype analysis showed any association to the STAT-1 gene in the Dutch coeliac disease population.
- Findings suggest that serine-phosphorylated STAT1, as a downstream target of protein kinase CK2, plays a critical role in the pathogenesis of Wilms' tumor and possibly other neoplasms with similar STAT1 phosphorylation patterns.
- This paper describes a previously unknown link between hypoxia and STAT1 expression down-regulation.
- link between HIF-1 and STAT1 reveals a previously unknown role of STRA13 in hypoxia and carcinogenesis
- STAT1 alpha overexpression increases cell apoptosis and Fas ligand expression, compared with STAT1 beta overexpression and enhance release of cytochrome c from the mitochondria and caspase-3 activity.
- Phosphorylation in trophpoblasts or blood mononuclear cells are activated with lipopolysaccharide or phytohemagglutinins.
- Our data suggest that ATRA-induced regulation of Stat2, ICSBP and C/EBPepsilon is dependent on active Stat1, and that a failure to correctly regulate these transcription factors is associated with the inhibition of monocytic differentiation.
- STAT1 deficiency caused by mutations Q463H and E320Q which affect STAT1 DNA-binding activity.
- observed a reperfusion time-dependent increase in the tyrosine phosphorylation of STAT1 and STAT3 at residues 701 and 705, respectively, which was dramatically reduced by tempol
- binding of HCV core to STAT1 results in decreased P-STAT, blocks STAT1 heterodimerization to STAT2, and, therefore, reduces IFN-stimulated gene factor-3 binding to DNA and disrupted IFN-stimulated gene transcription
- Stat1 exerts an inhibitory effect on early growth response (Egr)-1 gene and PDGF ligand mRNA transcription.
- These results suggest that RSV can inhibit the phosphorylation of IFN-alpha-inducible STAT1 and STAT2 by inducing the expression of SOCS proteins in PMA-treated U937 cells.
- the amount of IFN-gamma-induced STAT-1 activation in C. psittaci infected cells paralleled that observed in uninfected cells, suggesting that STAT-1 activation by these newly expressed receptors was impaired.
- STAT-1alpha, especially Ser(727) pSTAT-1, may function as a key molecule in the pathogenesis of Sjogren syndrome
- Expression of STAT1 in tumor-associated macrophages is an important independent prognostic factor for shorter overall survival in follicular lymphoma.
- When the tyrosine-phosphorylated STAT1 disengages from DNA, the N-terminal domain (ND) dimerizes and somehow assists in freeing the reciprocal binding between the monomers of the dimer while ND ND dimerization persists.
- These data suggest a mechanism of IC-mediated inhibition of IFN-gamma signaling, which requires the ITAM-containing FcgammaRI, as well as the ITIM-dependent phosphatase SHP-1, ultimately resulting in the suppression of STAT1 phosphorylation.
- using choriocarcinoma cells, it is shown that tyrosine phosphatase mediated suppression of IFN-gamma-inducible JAK and STAT-1 and select IFN-gamma-inducible gene expression in trophoblast cells may contribute to fetal maintenance
- Stat1 does not couple to apoptosis of A549 non-small cell lung adenocarconima cells.
- products of the rabies virus P gene are able to counteract IFN signaling by creating both cytoplasmic and nuclear blocks for STAT1.
- STAT1 and TA-p73 can interact directly, and p73-mediated Bax promoter activity was observed to be reduced by STAT1 expression in a p53-independent manner for which STAT1 Tyrosine-701 and Serine-727 are key residues.
- TGF-beta rapidly suppresses IFN-gamma-driven STAT1 signaling by reducing DNA binding via promotion of STAT1--PIAS1 interactions and not inhibition of STAT1 activation.
- Non-tyrosine phosphorylated-Stat1 is involved in a cooperative interaction with Spi-1/PU.1 and IRF8 in the formation of a pre-associated, poised complex for interleukin 1-beta gene induction.
- Stat1 in complex with Stat3 and HSF1 bound at the GAS element led to a moderate heat shock induction, designated as an "intrinsic" induction of the hsp90alpha gene; a changed level of heat shock induction was also controlled by the Stat1 on hsp90alpha.
- A mutation in STAT2 that confers an apoptotic effect in tumor cells in response to type I interferons, is described.
- interferon-induced STAT1 activation is enhanced by EBNA1
- This study represents the first microarray analysis for LQTS and implicates STAT1 in the pathogenesis and progression of LQTS and heart failure.
- STAT1 is required for interferon-inducible but not constitutive responsiveness to extracellular dsRNA.
- presence of intracellular HCV antigens led to transcriptional and protein expression of IL-8 (CXCL-8), and impaired interferon induction of signal transducers and activators of transcription 1 (STAT1) serine and tyrosine and STAT2 tyrosine phosphorylatio
- Results suggest that a PLCgamma-STAT1 pathway mediates apoptotic signaling by FGFR3 in genetic dwarfism and chondrogenic cell lines.
- Retention of import factors at the ER/Golgi membrane leads to a loss of STAT1 transport into the nucleus in response to interferon signaling, thus blocking the expression of STAT1-activated genes that establish an antiviral state.
- IFNalpha induces TRAIL expression via a STAT-1/IRF-1-dependent mechanism in human bladder cancer cells
- the V protein of SV5 functions as a bipartite adaptor linking DDB1 to STAT2, which in turn binds STAT1 and presents STAT1 to the E3 ligase complex for ubiquitination and subsequent degradation.
- STAT1 gene is expressed in an individual and specific manner both in HPV-positive cervical tumors and cell lines harboring transforming genes of these viruses.
- Mealse virus V protein can block the direct phosphorylation of STAT1 by Jak1 to escape IFN alpha/beta signaling.
- The onset of chromatin remodelling corresponds with the binding of activated STAT1 and the chromatin remodelling enzyme BRG1 at specific sites within the MHC, and is followed by RNA-polymerase recruitment and histone hyperacetylation.
- STAT1 decoy oligonucleotides were also used to block STAT1 mRNA and led to a decrease in the levels of STAT1 and to subsequence decrease in the percentage of apoptosis induced by Diallyl disulfide in examined colo 205 cells
- TNF-alpha leads to stabilization of IFN-epsilon mRNA, increased IFN-epsilon synthesis, engagement of type I IFNRs, increased STAT1 expression and phosphorylation, and up-regulation of retinoic acid-inducible gene-I expression
- Ser727 has a critical role in co-ordination of STAT1 functions in cellular responses
- EGFR induces expression of IRF-1 via STAT1 and STAT3 activation leading to growth arrest of human cancer cells
- These findings suggest that Ebola virus VP24 inhibits interaction of PY-STAT1 with karyopherins alpha1, alpha5, or alpha6 by binding within the PY-STAT1 binding region of the karyopherins.
- The induction of IFIT4 transcription by IFN-alpha depends upon sequential activation of PKCdelta, JNK and STAT1, and the influence of PKCdelta or JNK on IFN-alpha-mediated induction of IFIT4 is dependent upon the phosphorylation of STAT1 at Ser-727.
- Following cell exposure to IL-15, phosphorylation of STAT5 was predominantly observed, whereas, following stimulation with IL-21, there was predominant STAT1 and STAT3 activation.
- The polymorphism C39134A, located in a potentially cis acting regulatory element in STAT1 intron 24, was inversely related to total IgE levels and atopic sensitization in German children.
- psoriasin expression is transcriptionally suppressed by IFN-gamma; this effect is likely to be mediated by the activation of the STAT1 signaling pathway
- STAT1 plays an integral role in HIV-1-induced blood brain barrier damage and is relevant to viral neuropathogenesis.
- Induction of XAF1 by IFNbeta was mediated by the transcription regulator Stat1 through the ISRE site within the promoter region of XAF1 gene in colon cancer.
- Data demonstrate that human metapneumovirus can inhibit the interferon-alpha response through regulation of STAT1 phosphorylation, and provide important insight into the viral pathogenesis of hMPV infection in the respiratory tract.
- 22 out of 46 glioblastomas (48%) were strongly positive for staining with a STAT-1 antibody.
- results show that IL-15 can improve the function of NK cells via up-regulating NKG2D expression, and also augmenting the expression of cytotoxic effector molecules and the phosphorylation of STAT1 and ERK1/2, which may also contribute the NK lysis
- STAT-1 is involved in the signal transduction mechanism associated with cysteinyl leukotriene receptor 1 activation, supporting the hypothesis that it may represent a key transduction pathway leading to enhanced eosinophil adhesiveness.
- With maturation of melanocytes from junctional into dermal components of nevi, pSTAT1 expression increased, whereas pSTAT3 expression decreased.
- data show that genetic variants in the IRF-1 and Stat1 genes of the IFN pathway are associated with multiple sclerosis and hepatitis c virus infection.
- Stat1/3 directly controls promoter P1 of the CASR, and the Stats indirectly regulate promoter P2 of the CASR via Sp1/3 in response to IL-6
- These data define the role of the ISGF3 members in IFN-beta inhibitory signaling.
- KAP1 interacts with STAT1 and regulates IFN/STAT1-mediated IRF-1 gene expression in collaboration with HDACs.
- Although STAT1 phosphorylation required JNK and p38MAPK activation, only JNK activation was essential for IRF1 promoter activation by Tie2-R849W.
- IL-27 activates monocytes via STAT1 and suppresses IL-10 production but the inflammatory functions of IL-27 are abrogated by TLRs and p38
- Epstein-Barr virus SM protein induces splicing of STAT1 at a novel 5' splice site, resulting in a STAT1 mRNA incapable of producing STAT1 alpha.
- persistent activation of STAT1, STAT3, and STAT5 correlate with resistance to vorinostat in lymphoma cell lines
- Fludarabine, an antileukemic drug active against cells that express STAT-1, selectively kills M. avium-infected macrophages.
- JAK/STAT-1 signaling pathway was necessary and sufficient to mediate the down-regulation of FcRn gene expression by IFN-gamma
- STAT1-dependent pathway is not essential for repression of ICPO-null mutant herpes simplex virus type 1 in fibroblasts.
- STAT1 constantly oscillated between different dimer conformations, whereby the abundance of the dimerization interfaces was determined by tyrosine phosphorylation.
- ISRE, STAT1, and STAT2 have essential roles in the regulation of constitutive and IFN-alpha-mediated PD-1 expression in macrophages
- Results reveal that nuclear beta-arrestin1, acting as a scaffold for the dephosphorylation of STAT1, is an essential negative regulator of IFN-gamma signaling and participates in the IFN-gamma-induced cellular antiviral response.
- The relationship of histone methylation at distal and proximal regulatory elements was characterized by comparing ChIP-seq profiles for these histones and for STAT1 in the immortalized HeLa cell line, with and without interferon-gamma stimulation.
- Iron chelators and hypoxia mimetics inhibit IFNgamma-mediated Jak-STAT signaling
- Evidence for a role of STAT1 in genetic susceptibility to SLE was not detected
- STAT1 plays an important role in hyaluronan -mediated inflammatory processes.
- SHP2 activation induced by HCMV infection is responsible for the down-regulation of IFN-gamma-induced STAT1 tyrosine phosphorylation.
- influenza A viruses suppress type I IFN signaling on the level of JAK/STAT activation
- The authors mapped STAT1 binding site in the N-terminal region of measle virus V protein and identified a minimal peptide of only 11 amino acids.
- human colon carcinoma cells silence IFN-gamma-activated IRF8 expression through MBD1-dependent and PIAS1-mediated inhibition of pSTAT1 function at the methylated IRF8 promoter
- STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage.
- This is the first study reporting the overexpression of STAT1 in human clear cell and papillary RCC tissues.
- STAT1-activating cytokines interleukin (IL)-27 and interferon (IFN)-gamma amplify transforming growth factor (TGF)-beta-induced FOXP3 expression.
- findings identify PRMT1 as a novel and crucial negative regulator of STAT1 activation that controls PIAS1-mediated repression by arginine methylation
- STAT1 acetylation induces binding of TCP45, which catalyzes dephosphorylation and latency of STAT1