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Validated All-in-One™ qPCR Primer for STAT3(NM_139276.2) Search again
Product ID:
HQP017768
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADMIO, ADMIO1, APRF, HIES
Gene Description:
signal transducer and activator of transcription 3
Target Gene Accession:
NM_139276.2(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 is activated through phosphorylation in response to various cytokines and growth factors including IFNs, EGF, IL5, IL6, HGF, LIF and BMP2. This protein mediates the expression of a variety of genes in response to cell stimuli, and thus plays a key role in many cellular processes such as cell growth and apoptosis. The small GTPase Rac1 has been shown to bind and regulate the activity of this protein. PIAS3 protein is a specific inhibitor of this protein. Three alternatively spliced transcript variants encoding distinct isoforms have been described. [provided by RefSeq].
Gene References into function
- dysregulation of STAT3 activation in anaplastic lymphoma kinase-positive T/null-cell lymphoma
- Modulation of signal transducer and activator of transcription 3 activities by p53 tumor suppressor in breast cancer cells.
- Cytokine signaling: STATS in plasma membrane rafts
- actdivated by fiboblst growth factor 3 and adapter protein SH-B
- Stat1 and Stat3 may support cell growth in part via c-myc gene activation in primary erythroleukemia cells.
- inhibits gamma-globin gene expression in erythroid cells.
- Breast Carcinoma cell growth could be inhibited by dominant-negative versions of STAT3.
- STAT3 isoforms are differentially expressed and phosphorylated during progression of granulocytic differentiation.
- The C-terminal domain of Stat3 negatively regulates its receptor binding activity only in the absence of the first alpha-helix of the coiled-coil domain, which leads to a hypothesis of intramolecular interaction.
- The transforming capacity of constitutively activated STAT3 and STAT5 mutants strongly supports their fundamental role in the process of malignant transformation in hematopoietic cells
- IL-6-inducible expression of the hAGT promoter is mediated by physical association of the COOH terminus of STAT3 with p300/CBP, the recruitment of which targets histone acetylation and results in chromatin remodeling.
- STAT5b-RARalpha and other APL fusion proteins may contribute to leukemogenesis by interaction with the STAT3 oncogene pathway.
- Phosphorylation of STAT-3 in response to basic fibroblast growth factor occurs through a mechanism involving platelet-activating factor, JAK-2, and Src in human umbilical vein endothelial cells
- Reproductive hormone-induced, STAT3-mediated interleukin 6 action in normal and malignant human ovarian surface epithelial cells.
- Constitutive Stat3 activity up-regulates VEGF expression and tumor angiogenesis
- Stat3 activity is significantly increased in both prostate cancer and adjacent normal prostate tissue; activation may be an early event in prostatic epithelial carcinogenesis
- Stat3 and GRP58 were observed to be coassociated with cytoplasmic membranes
- activated in human ovaarian carcinoma; co-expressed with oncostatin M and its receptor
- Constitutive activation of signal transducers and activators of transcription 3 correlates with cyclin D1 overexpression and may provide a novel prognostic marker in head and neck squamous cell carcinoma.
- activation by type I interferons is dependent on specific tyrosines located in the cytoplasmic domain of interferon receptor chain 2c
- STAT3 is activated by HGF/HGFR and has a role in fetal organogenesis and placental tissue
- constitutive STAT3 activation contributes to tumor growth in SCCHN, independent of the EGFR autocrine axis.
- Data show that IL-6/raft/STAT3 signaling is a chaperoned pathway that involves caveolin-1 and HSP90 as accessory proteins and suggest a mechanism for the preservation of this signaling during fever.
- The nuclear isoform of protein-tyrosine phosphatase TC-PTP regulates interleukin-6-mediated signaling pathway through its dephosphorylation.
- PKC delta associates with IL6ST via Stat3 and enhances Stat3-gp130 interaction
- Platelet signaling pathways activated by thrombopoietin may affect mitochondrial transcription via activation of mitochondrial STAT3
- findings suggest that activated STAT3 signaling directly contributes to malignant progression of primary effusion lymphoma by preventing apoptosis, acting through the prosurvival protein survivin
- selectively activated in immature dendritic cells by expression of HIV nef
- Schwannomin and HRS inhibit Stat3 activation in schwannoma cells.
- ablation of Stat3 function converts EGF from a growth/survival factor for RA synoviocytes to a death factor
- Inhibition suppresses proliferation and induces apoptosis in glioblastoma multiforme cells
- Dysregulated STAT3 activity by PML/RAR alpha may participate in the pathogenesis of APL.
- Kaposi sarcoma-associated viral cyclin K overrides cell growth inhibition mediated by oncostatin M through inhibition of this protein.
- Stat3 directly regulates VEGF expression and hence angiogenesis, growth, and metastasis of human pancreatic cancer
- expression and DNA-binding activity of this protein in alcoholic cirrhosis compared to normal liver and primary biliary cirrhosis in humans
- identification of tip60 as a co-repressor for STAT3
- inhibition by differentiation-inducing factor-1 is involved in gastric cancer cell proliferation via MEK-ERK-dependent pathway
- This protein is activated by leptin which activates the FAAH promoter in T cells.
- Ataxia telangiectasia mutated proteins, MAPKs, and RSK2 are involved in the phosphorylation of this protein.
- THE presence of this protein and its phosphorylated derivative in node-negative breast cancer shows nuclear localization is associated with a better prognosis.
- independent and cooperative activation of chromosomal c-fos promoter by STAT3
- STAT3 is constitutively activated in Crohn's patients but not in healthy volunteers
- Hematopoietic CD34+ cells secreted IL-15 that, through autocrine/paracrine loop distinct signal pathways, activated NF-kB in bone marrow and cord blood progenitors, and activated STAT3 and STAT5 in peripheral G-CSF-mobilized and BM progenitors only.
- GRIM-19 protein specifically suppresses Stat3 protein activity via functional interaction.
- gp120 induces activation of STAT1, STAT3, and STAT5 in CD4+ cells of lymphocyte or monocyte/macrophage lineages.
- We conclude that IL-6 may promote cervical tumorigenesis by activating VEGF-mediated angiogenesis via a STAT3 pathway.
- activation of STAT3 was dependent on Ser727 phosphorylation, in the absence of detectable Tyr705 phosphorylation; expression of human STAT3 in murine macrophages rescued inhibition of human Mcl-1 promoter gene activation and cell death induced by NaSal
- RET/PTC associates with STAT3 and activates it by the specific phosphorylation of the tyrosine 705 residue. STAT3 activation by the RET/PTC tyrosine kinase is one of the critical signaling pathways for the regulation of specific genes.
- Inhibition of this protein with a decoy oligodeoxyribonucleotide abolishes head and neck cancer cell growth.
- G protein-coupled receptors activate STAT3 via G alpha(16), a G alpha subunit which is primarily expressed in hematopoietic cells.
- Analysis of this protein's pathway in myeloma: its activation and cyclin D1 dysregulation are mutually exclusive.
- ubiquitylation and degradation by mumps virus V protein prevents responses to interleukin-6 and v-Src signals and can induce apoptosis in STAT3-dependent multiple myeloma cells and transformed murine fibroblasts
- Results provide evidence that interleukin-13 induces p38 MAP kinase phosphorylation and activation, which regulates Stat1 and Stat3 serine 727 phosphorylation.
- 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.
- Epidermal growth factor receptor-independent constitutive activation of STAT3 in head and neck squamous cell carcinoma is mediated by the autocrine/paracrine stimulation of the interleukin 6/gp130 cytokine system.
- We now demonstrate ligand-independent activation of Stat3 by high cell density in multiple cancer cell lines.Interference with cdk2 activity upregulates Stat3 phosphorylation and Stat3-directed DNA-binding activity.
- AR and PIAS3 regulate the STAT3-mediated transcriptional activity by their physical protein-protein competition on STAT3
- STAT3 has a role in the pathogenesis of human chronic myelogenous leukemia
- Stat1 and Stat3 exist as stable homodimers prior to activation
- Stat3 has a role in transducing survival signals downstream of tyrosine kinases such as Src, EGF-R, and c-Met, as well as cytokines such as IL-6, in human nonsmall cell lung cancers
- 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.
- STAT3 activation associated with better disease-free survival in nasopharyngeal carcinoma
- STAT3 activation is required for keratinocyte differentiation in normal human stratified squamous epithelium
- Stat3 is transactivated via IL-6 response elements on fibrinogen promoters with participation of additional transcription factors
- Nef activates STAT3 through a mechanism mediated by the release of soluble factor(s) in human monocyte derived macrophages.
- Differentiation-dependent expression of STAT3 may modify responses to growth factors in the cancers of the head and neck.
- The activation of signal transducer and activator of transcription 3 (Stat3) is obligatory for the survival of INA-6 multiple myeloma cells.
- Signal transducer and activator of transcription 3 is the most potent activator of acute-phase gene transcription.
- STAT3 is stimulated by Galpha16 via a c-Src/JAK- and ERK-dependent mechanism
- STAT3/NF-kappaB p65 cross-talk activated by IL-1 via TRAF6.
- role in regulating expression of hepatocyte growth factor
- Specific DNA binding activity of two STAT3 variants (STAT3alpha and beta) was observed in immature trophoblasts and appeared to be lost in term placentae. The malignant phenotype of choriocarcinoma cells coincides with a high degree of STAT3 activity.
- Although the data show that STAT3 is required for the majority of IL-10 functions, there are elements of the anti-inflammatory activity of IL-10 that are STAT3 independent.
- STAT3 recombinant fusion protein shuttles continuously between the cytosol and the nucleus in unstimulated cells
- interaction of Stat3 and ZBP-89 may be crucial for overcoming the effects of the repressor ZBP-89, which suggests a novel mode for Stat3 gene activation.
- In the luciferase assay, ATBF1 was found to have no influence on STAT3 signaling induced by IL-6 stimulation, but it did synergistically enhance PIAS3 inhibition of activated STAT3.
- Taken together, our findings demonstrate that constitutively activated Stat3 up-regulates HSP27 and may facilitate phosphorylation of HSP27 at serine residue 78.
- G-CSF like IL-10 inhibits LPS-induced TNF-alpha production in human monocytes through selective activation of STAT3 and the immunomodulation observed in vivo by G-CSF administration may be partly ascribed to the direct effect of G-CSF on monocyte functio
- MITF and STAT3 cooperatively induce c-fos, resulting in cellular transformation
- STST3 activation is mediated by EGFR and c-Src and facilitated by Pyk2
- interactions of the phosphotyrosine ligands with specific amino acid residues of Stat3 SH2 region are described
- Stat3 activity is upregulated during the confluence-mediated growth arrest by a signalling mechanism that requires JAKs
- IL-10 gene regulation in colon tumor cells is mediated by STAT3, which is phosphorylated after the binding of IL-6 the IL-6 receptor.
- N-(3-oxododecanoyl)-L-homoserine lactone (OdDHL) from P. aeruginosa ablates STAT3 activity in breast tumor cells.
- cells from multiple myeloma patients express constitutively active NF-kappaB and STAT3, and suppression of these transcription factors inhibits the survival of the cells
- STAT3 signaling supports gastric cancer cell survival in association with survivin expression.
- a profound in vivo activation of STAT3 is observed in mycosis fungoides (MF) tumors but not in the early stages of MF. STAT3 protects tumor cells from apoptosis in vitro. Taken together, these findings suggest that STAT3 is a malignancy factor in CTCL.
- the c-src kinase/STAT3 pathway has a role in Ox-PAPC-mediated IL-8 expression in endothelial cells
- STAT3gamma is rapidly generated from STAT3alpha by limited proteolysis with granule-derived serine proteases during preparation of neutrophil lysates
- Inhibition of STAT3 reduced the motility of ovarian cancer cells in vitro, and activated STAT3 localized not only to nuclei but also to focal adhesions in these cells.
- STAT3 directly contributes to the high level of TIMP1 expression in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
- Constitutive activation of Stat3 may play an important role in the tumorigenesis of colorectal carcinoma
- results show STP-A11 (Saimiri transforming protein oncogne of Herpesvirus saimiri subgroup A strain 11) independently targets two important cellular signaling molecules, Src and Stat3; these proteins cooperate to induce STP-A11-mediated transformation
- expression of STAT-3 induced by Epstein-Barr virus (EBV) LMP-1 (latent membrane protein) and may be part of the viral programming that regulates viral latency and cellular transformation
- constitutive activation of Akt and NFkappaB, but not Stat3, contributes significantly to the progression of diffuse gliomas
- importance of STAT3 signaling in the regulation of neuronal growth and differentiation by the mu-opioid receptor.
- Although the methylation frequency of SOCS-1 is low, the data of Fujitake et al. indicate role of JAK/STAT/SOCS pathway in gastrointestinal tumorigenesis.
- We found that the amino terminal domain of STP A11 is required for both STAT3 interaction and activation, and that physical interaction is required for STAT3 activation.
- STAT3 interacts with STRA13 and modulates transcription of STAT3-dependent targets.
- Inhibition of Stat3 activity by TEL represents a novel mechanism regulating the Stat3 signaling pathway
- Stat3 mediated by c-Met is frequently associated with the progression of oral squamous cell carcinoma
- Existence of a factor in mouse feeder layer cells that acts to maintain huma embyonic stem cells cell renewal in a STAT3-independent manner.
- data reveal an important role for MgcRacGAP in STAT3 activation, and demonstrate that MgcRacGAP regulates IL-6-induced cellular differentiation in which STAT3 plays a pivotal role
- Promotes the initiation of transcription but also regulates chromatin remodeling and transcription elongation through its interaction with BRG1 and cdk9.
- Detailed pathway analysis revealed that BM stromal cells stimulate STAT3 via the IL-6R, and MEK1/ERK1 pathways, via IL-6R-independent mechanisms
- STAT3 forms a related complex in cells upon oxidative stress. interacting at cysteine 259.
- constitutively active Stat3 upregulates MEK5 in the breast epithelial cells. MEK5 may be one of the Stat3-regulated genes and plays its essential roles in oncogenesis
- STAT3 activation is capable of initiating intracellular antiviral pathways
- Growth hormone attenuates the transcriptional activity of Runx2 by facilitating its physical association with Stat3beta
- Ectopic expression of wild-type but not Thr(p+1loop)-->Met substituted EPH family members constitutively phosphorylated STAT3
- The conserved STAT3 region from 752 to 761, called STAT3 CR2, plays critical roles in STAT3-dependent transcription by recruiting SRC-1 and allowing Ser727 phosphorylation.
- Cold ischemia and reperfusion induced increased levels in liver transplantation.
- The STAT3 was detected in cytoplasm and nucleus and in carcinomas it was limited to cytoplasm.
- Coordination between Stat1 & Stat3 activation determines GTPCH I induction. Stat1 & NF-B activation, coordinated with the lack of Stat3 activation, accounts for cytokine-stimulated GTPCH I induction in endothelial cells.
- The N-terminal part of the 1st intracellular loop (ICL) is needed to activate Jak2 after SDF-1alpha binding to CXCR4, leading to phosphorylation of only one cytoplasmic Tyr, present at the C terminus of the 2nd (ICL), which triggers STAT3 activation.
- suppressor of cytokine signaling 3 regulates Hepatocyte growth factor-induced keratinocyte migration by inhibiting STAT3 phosphorylation
- an increased transcriptional level of constitutive STAT3 may be related to the suppressive regulation of the apoptotic pathway in intrinsically chemo-resistant NSCLC cells.
- acetylation of Stat3 can stimulate its sequence-specific DNA binding ability and transactivation activity.
- results show that Hepatitis C virus(HCV)-induced activation of STAT-3 is mediated by oxidative stress and influenced by the activation of cellular kinases; results also suggest a potential role of STAT-3 in HCV RNA replication
- Lys685 acetylation critical for Stat3 to form dimers required for cytokine-stimulated DNA binding & transcriptional regulation, to enhance transcription of cell growth-related genes & to promote cell cycle progression after treatment with oncostatin M
- one of the major roles of Stat3 in the G-CSF signaling pathway is to augment the function of C/EBPalpha, which is essential for myeloid differentiation
- TFF3 and the essential tumor angiogenesis regulator VEGF(165) exert potent proinvasive activity through STAT3 signaling in human colorectal cancer cells.
- Results indicate that SOCS-7 is a dysregulator of prolactin, leptin, and growth hormone signaling and that its mode of action is a variation of SOCS protein inhibition of cytokine-inducible STAT3 and 5-mediated signal transduction.
- Over-expression of VEGF may be correlated with elevated STAT3 activation in parental cell line
- IL-6-induced STAT3 activation in human prostate cancer cell lines.
- HIF-1alpha, STAT3, CBP/p300 and Ref-1/APE regulate Src-dependent hypoxia-induced expression of VEGF in pancreatic and prostate carcinomas
- pharmacological agents that can selectively reduce the P-STAT3 levels in human cancer cells result in tumor apoptosis and growth inhibition
- previously uncharacterized genes induced by Stat3 implicated in signaling pathways common to both wound healing and cancer including cell invasion and migration, angiogenesis, modulation of coagulation, and repression of interferon-inducible genes
- Findings provide evidence that STAT 3 signal activity in head and neck carcinomas, which is partially responsible for proliferative activity, can be controlled via the EGFR.
- STAT3 enhances the efficiency of its own Ser-727 phosphorylation by acting as a scaffold for the TAK1-NLK kinases
- extracellular signal-dependent nuclear transport of STAT3 is mediated by various importin alphas, importin beta, and Ran
- demonstrate using RNAi that Stat3 activation is necessary in the invasive phenotype of trophoblast cells and can be controlled via Leukemia Inhibitory Factor (LIF)
- cIAP2 expression is up-regulated by IFN-alpha and IFN-gamma through the JAK2-STAT3 pathway, and increased expression of the cIAP2 protein may contribute to an IFN-alpha- and IFN-gamma-mediated antiapoptotic effect on human neutrophils.
- STAT3 may transform cells by inducing epigenetic silencing of SHP-1 in cooperation with DNMT1 and histone deacetylase 1
- interacts with dengue-2 virus NS1 protein
- activation by leptin is associated with gastric cancer cell proliferation
- STAT3 signaling pathway is involved in IL-6-induced neuroendocrine(NE) differentiation and that p38 MAPK is associated with IL-6-stimulated growth regulation in NSCLC-NE cells.
- The physiological role of Stat3 in anaplastic large cell lymphomas and the effects of inhibition of expression of the gene on tumorigenesis is reported.
- Activation of Stat3 signaling in respiratory epithelial cells of STAT3 transgenic mice protects against hyperoxia-induced inflammation and injury in the lung.
- STAT3 signaling is important in the pathogenesis of classical Hodgkin lymphoma
- Stat3 is an important component of a pathway emanating from tumor antigen of Simian Virus and leading to neoplastic conversion
- Data show that medroxyprogesterone acetate treatment of mammary tumor cells up-regulated Stat3 protein expression and induced rapid, nongenomic Stat3, Jak1, and Jak2 tyrosine phosphorylation.
- Our results indicate that genetic variants in STAT3, independent of asthma treatment, are determinants of FEV1 in both adults and children with asthma.
- These suggest that JNK and STAT3 may constitute a universal signaling pathway to mediate adiponectin's pathophysiological effects on metabolic syndrome and cancer.
- Janus kinase Tyk2 and the transcription factor Stat3 serve as downstream components in the signaling cascade resulting in upregulation of C5aR expression
- STAT3 physically interacts with epidermal growth factor receptor in the nucleus, leading to transcriptional activation of inducible nitric oxide synthase.
- Results identify a cohort of STAT3 targets that may mediate its role in oncogenesis in breast and prostate cancer.
- 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
- Stat3 is required for both basal and growth signal-induced expression of HIF-1
- STAT3 has a role in colorectal tumor growth
- Growth factors and cytokines stimulate hTERT expression in primary human cells in a STAT3-dependent manner. STAT3 is a key regulator of hTERT expression in both normal and tumor cells.
- Association between STAT3 and ARHI as well as the functional inhibition of STAT3 transcriptional activity by ARHI suggests a novel mechanism through which a putative tumor suppressor gene can inhibit STAT3 activity in breast and ovarian cancers.
- constitutive Stat3 signaling may be one of the key upstream regulators to induce downstream proteins which may play important roles in Stat3-mediated oncogenesis in breast cancer
- STAT3 can participate in neoplastic transformation through novel and non-canonical mechanisms [review]
- End-stage hepatitis c and alcoholic liver cirrhosis is characterized by impaired Stat3 DNA-binding possibly through up-regulation of Pias3.
- repression of tumor protein p53 expression by Stat3 is likely to have an important role in development of tumors
- Results suggest a connection between leukemia inhibitory factor-driven STAT3 activity and invasiveness of choriocarcinoma and trophoblast cells.
- These data demonstrate that Arg-214/215 are involved in CRM1-mediated STAT3 nuclear export and the regulation of STAT3 activity.
- NF-kappaB and STAT3 are activated by proteolysis inducing factor in human Kupffer cells and monocytes
- AKT1 is a direct target gene of Stat3 and contributes to Stat3 anti-apoptotic function
- Inhibition of STAT3 signaling in colon carcinoma tumors and cell lines induces apoptosis and cell cycle arrest of colon carcinoma cells.
- We provide evidence that STAT3 plays an essential role in cytokine-driven SAA expression, although the human SAA gene shows no typical STAT3 response element
- Cyclooxygenase-2-dependent activation of STAT3 by interleukin-6 has a role in non-small cell lung cancer
- acetylation-deacetylation reaction as a novel signaling mechanism controlling the IL-6-STAT3 pathway in the hepatic acute phase response
- STAT3-mediated transcriptional activation in inhibited by Daxx
- Stat3 downregulation in vSrc transformed NIH3T3 cells or in breast cancer lines with activated Src induces apoptosis, but in normal cells Stat3 inhibition at post-confluence causes apoptosis while in sparsely growing cells it induces growth retardation
- STAT3 and PY-STAT3 in the cytoplasm have roles in endocytosis
- Our results suggest that p-ser727-STAT3 may be involved in the pathogenesis of breast cancer in an ER-dependent manner.
- SOCS-1 methylation status can differentially affect STAT3 activation
- This review of head and neck squamous cell carcinoma discusses how STAT3 alters the tumor cell cycle, prevents apoptosis, and mediates proliferation and survival of tumor cells.
- findings demonstrate that Stat3 plays a critical role in the tumorigenesis, but not in the cell survival, of cutaneous squamous cell carcinoma cells and suggest that additional pro-apoptotic signals are necessary for the induction of apoptosis
- there are tissue-specific differences in IL-6-receptor-gp130-coupled signaling which limit the extent of Stat3 activation and gammaFBG expression during lung inflammation
- Tax-mediated regulations of IL-6R and sIL-6R observed in HTLV-I-associated disorders may contribute to proliferation of HTLV-I-infected T cells through activation of inducible STAT3
- Activation requires the catalytic activity of Brk.
- 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
- Stat3 is involved in keloid pathogenesis. Inhibitors of Stat3 may be useful therapeutic strategies for the prospective treatment of keloid scars.
- Stat3 undergoes proteolytic processing by caspases that reduces its expression and leads to the formation of cleavage fragments that may modulate Stat3 transcriptional activity
- Stat3-mediated p100 processing to p52 requires activation of Stat3 by the acetyltransferase activity of cAMP-response element-binding protein (CREB)-binding protein (CBP)/p300
- To our knowledge, this is the first study on the poor prognosis of p-STAT3 in human colorectal adenocarcinomas. These findings suggest that expression of p-STAT3 is related to tumour invasion and poor prognosis of human colorectal adenocarcinoma.
- role for IL-11 via pSTAT3 and SOCS3 in initiating and progressing decidualization
- Silencing Stat3 expression by small interfering RNA (siRNA) abrogated BCL3 expression by IL-6
- Haplotypes of STAT3 predict cardiovascular disease in renal dialysis patients.
- Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
- Atiprimod blocked Stat3 activation and inhibited colony-forming cell proliferation in acute myeloid leukemia cells.
- Mechanism by which hepcidin can be regulated by inflammation or, in the absence of inflammatory stimuli, by alternative mechanisms leading to STAT3 activation.
- IL-6 induces Protein S expression via STAT3. Possible function for IL-6-induced Protein S expression in cell survival.
- STAT3 activation by IL-6 provides an antiapoptotic advantage in human cord blood cells CD34+ cells, essentially owing to the expression of bcl-2.
- STAT3 binds in vitro to 2 STAT3 SIE/GAS-binding sites identified in promoter 1 and enhancer 1 of the DNMT1 gene
- mutant JAK2 contributes to myelofibrosis with myeloid metaplasia pathogenesis by constitutively phosphorylating STAT3 and diminishing myeloid cell apoptosis
- These reuslts show a significant association between the expression of the phosphorylated/active form of STAT3 (pSTAT3) and that of TIMP1.
- Stat3 binding at position -1024 of the endothelial nitric-oxide synthase (eNOS) promoter mediates Stat3 inhibition of eNOS promoter activity.
- Phosphorylation in trophoblasts or blood mononuclear cells activated with lipopolysaccharide or phytohemagglutinins showed phosphorylation of this protein.
- PDTC downregulates IL-6-induced STAT3 activation by altering the stability of STAT3-Hsp90 complex
- 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
- STAT3 is a key effector of baseline hepcidin expression and during inflammatory conditions.
- results suggest that phospho-Stat3 expression might be associated with angiogenesis, anti-apoptosis, and tumor progression in gastric cancer
- The activated (phosphorylated) Stat3 is overexpressed in most paclitaxel-resistant ovarian cancer cells. The interruption of Stat3 signaling could reverse resistance to paclitaxel and perhaps other chemotherapy agents in human cancer.
- These results suggest a relevant role for STAT5 and Bcl-xL as apoptosis-regulatory proteins in the pathogenesis of lung cancer, and overexpression of both Neu and activated STAT3, could be related with the proliferation rate in lung carcinoma cells.
- there is a cross-talk between the NFkappaB and the STAT3 signaling systems, and HNSCC may result from the aberrant activity of a signaling network
- STAT3 activation by G alpha(s) distinctively requires protein kinase A, JNK, and phosphatidylinositol 3-kinase
- The Ras/Raf-1/MEK1/ERK cascade culminates in nicotine up-regulated expression of the gene encoding STAT-3, whereas recruitment and activation of tyrosine kinase JAK-2 phosphorylates it.
- To determine the prosurvival function of STAT3 vs STAT5 within the same tumor model, genes were profiled in STAT3- or STAT5-depleted human lymphoblastic lymphoma-derived cell line YT cells by apoptosis-specific microarrays
- Chromium activates epithelial cell Lck to signal for prolonged STAT3 activation and transactivation of interleukin-6, an important immunomodulator of lung disease progression
- Leptin and TGF-beta1 synergistically augmented activation of signalling components of mitogen-activated protein kinase (MAPK), STAT3 and Smad but did not modulate the expression of LEPR-B.
- The STAT3 pathway is involved in Cdk5-dependent proliferation of medullary thyroid cancer cells through Ser-727 phosphrylation.
- Activated STAT3 translocates to the nucleus of KSHV-infected endothelial cells, where it can bind to STAT3-specific DNA elements and can activate STAT3-dependent promoter activity.
- BRG1 is constitutively present at IL-6-responsive promoters and is required for STAT3 recruitment, downstream histone modifications, and IL-6-induced chromatin remodeling.
- STAT3 activity can suppress both IL-6 and tumor necrosis factor production in lipopolysaccharide-stimulated macrophages.
- activation of STAT3 may play an important role in the tumorigenesis of gastric adenocarcinoma
- These data suggest that STAT3 signaling is an important common element and may contribute to the remodeling and adaptation of skeletal muscle following resistance exercise.
- tumor samples from FMTC patients showed strong nuclear staining of phosphorylated ERK1/2 and Ser(727) STAT3; FMTC-RET mutants activate a Ras/ERK1/2/STAT3 Ser(727) pathway, which plays an important role in cell mitogenicity and transformation.
- let-7a modulates interleukin-6-dependent STAT-3 survival signaling in malignant human cholangiocytes
- SOCS-3 epigenetic silencing is responsible for sustained IL-6/STAT-3 signaling and enhanced Mcl-1 expression in cholangiocarcinoma
- Cell confluence-induced Stat3 signaling is induced in Madin-Darby canine kidney epithelial cells in triggering dome formation through sodium hydrogen exchanger-3 augmentation.
- Myocardial STAT3 protein levels are reduced and serum levels of activated cathepsin D and 16 kDa prolactin are elevated in postpartum cardiomyopathy patients.
- Stat3 is activated in human endometrial and cervical cancers and the inhibition of constitutive Stat3 signaling may be an effective target for cancer intervention in these two cancers.
- In chronic hepatitis C, liver fibrosis progression is characterized by a continuous decline in Stat3 DNA-binding activity related to overexpression and progressive interaction of Pias3-Stat3.
- STAT-3 activation by DFMO is at least in part mediated through the PKA pathway
- This review article discusses the role of STAT3 in cancer in detail as evidenced by its constitutive activity in tumor cells, and its regulation of genes that mediate proliferation, suppress apoptosis or promote angiogenesis.
- silibinin inhibits constitutively active Stat3 and induces apoptosis in DU145 cells, and thus might have potential significance in therapeutic intervention of this deadly malignancy.
- CYCLIN D1 may be a target gene for leptin mediated growth stimulation of breast cancer cells and molecular mechanisms involve activated Stat3
- STAT3 is a substrate of receptor protein tyrosine phosphatase T
- Increasing the protein levels of the signal transducer and activator of transcription 3 (Stat3) led to Stat3-androgen receptor (AR) complex formation in response to epidermal growth factor (EGF) and interleukin-6 (IL-6) stimulation.
- found 3 specific patterns of pSTAT-3 and pSTAT-5 expression: uniformly increased pSTAT-3 and pSTAT-5 expression in PV, increased pSTAT-3 and reduced pSTAT-5 expression in ET, and uniformly reduced pSTAT-3 and pSTAT-5 expression in IM.
- CCL2 mediates fibroblast survival by inhibiting apoptosis through IL-6/STAT3 signaling
- IL-10 induces IL-10 in monocyte-derived macrophages in an autocrine manner via activation of the transcription factor Stat3.
- Constitutively activated STAT3 induces tumorigenesis and enhances cell motility of prostate epithelial cells through ITGB6.
- Activation of the STAT3 signaling pathway plays an important role in the progression of pancreatic cancer, and silencing of the STAT3 gene with RNAi may be a useful anti-invasive therapeutic option in pancreatic cancer.
- Aberrant activity of STAT3 in colorectal neoplasms is linked to malignant tumor progression through upregulated expression of matrix metalloproteinases MMP-1, -3, -7, and -9.
- antitumor activity of S3I-201 is mediated in part through inhibition of aberrant Stat3 activation
- administration of IL-6 could activate receptor gp80/gp130 signaling pathways including downstream extracellular signal-regulated kinase 1/2 and STAT3 phosphorylation in EPCs.
- STAT3 and PKC differentially regulate telomerase activity during megakaryocytic differentiation of K562 cells.
- Blockade of the gp130 receptor or sequestration of the interleukin-6 (IL-6) ligand led to a decrease of phosphorylated Stat3 levels in breast cancer.
- GM-CSF-stimulated CD34(+) cell proliferation is regulated by the JAK/STAT3/survivin signaling pathway.
- in addition to activating NF-kappaB/p52, LIGHT also activates Stat3 through the NIK pathway
- These results indicate that expression of the gamma-fibrinogen gene is mainly controlled by the strength of late phase STAT3 activation, which in turn is negatively regulated by the extent of interleukin-1beta-mediated NF-kappaB activity.
- Stat3 has a role in the photodynamic reaction in cells and tumors
- The activation of MMP-9 promoter is dependent upon interactions of Fra-1/c-Jun with Stat3.
- Statistically analyzed distributions of the proteins reflected functional dependences among STAT3, HIF-1alpha, EPO and EPOR in cellular signal conduction.
- STAT3 polymorphism has a role in patient resopnse to IFN-alpha therapy in patients with metastatic renal cell carcinoma
- These observations suggest that SOCS6 is composed of at least two functional domains required for its biological role in localizing and degrading Stat3 in the nucleus.
- GRIM-19 suppresses constitutive STAT3-induced cellular transformation in vitro and in vivo by down-regulating the expression of a number of cellular genes involved in cell proliferation and apoptosis
- Since STAT3 reactivation occurred in 14 of 15 solid tumor cell lines, dasatinib combined with Janus-activated kinase inhibitors may have widespread application in cancer treatment.
- Amino acid residues required for physical and cooperative transcriptional interaction of STAT3 and AP-1 proteins c-Jun and c-Fos.
- Single nucleotide polymorphism variations are not indicative of obesity and insulin resistnce.
- In actinic cheilitis, STAT-3 expression depends on the degree of dysplasia, and STAT-3 activation is dysregulated compared with normal tissue
- Response rates to HCV-specific treatment are higher in HCV/HIV-positive patients carrying the IL-6 HP genotype, which might be because of IL-6 mediated STAT3 activation.
- Data provide direct evidence for IL-6 induced "signal transduction" by STAT3 from the plasma membrane to a cytoplasmic membrane destination for yet to be elucidated function(s) in the cytoplasm including prolongation of signaling and/or cross talk.
- STAT 3 and androgen receptor signaling are inactivated in androgen-dependent LNCaP cells after administration of Saw Palmetto
- dominant-negative mutations in the human signal transducer and activator of transcription 3 (STAT3) gene result in the classical multisystem hyper-immunoglobulin E syndrome (HIES)
- phosphorylated STAT3 and Akt play an important role in pathogenesis of malignant tumors of the epidermis
- Sodium arsenite dose dependently alters STAT3 and JAK2 activities via Bcl-6 and this may have a role in arsenic-associated carcinogenesis.
- Stat3 has an important role in the early stages of epithelial carcinogenesis as well as a novel role in malignant progression of skin tumors in a transgenic mouse model.
- STAT3, Runx2, and steroid receptor coactivator-1 are critical molecules in mediating leptin-stimulated cell osteogenesis in TOLF (thoracic ossification of ligament flavum)
- STAT3 tyrosine phosphorylation occurs in preformed transducer complexes that can be activated in the absence of intact lipid rafts or caveolin.
- The combined data suggest that STAT3 tyrosine phosphorylation occurs in preformed transducer complexes that can be activated in the absence of intact lipid rafts or caveolin.
- in angiosarcoma, significant correlation was seen between phosphorylated-STAT3 and cyclin D1 but not between phosphorylated Akt and cyclin D1
- The role of the STAT3 pathway in the regulation of IL8 transcription by Ox-PAPC in vitro and in atheroclerosis in vivo is reported.
- Inhibition of exportin-1-mediated nuclear export slowed down nucleocytoplasmic shuttling of v-Src-activated STAT3 resulting in reduced tyrosine phosphorylation, decreased induction of STAT3 target genes and increased apoptosis.
- ET Patients lacking the JAK2V617F mutation displayed significantly lower expression of the JAK/STAT target genes Pim-1 and suppressor of cytokine signaling-2. In addition, JAK2V617F-negative patients showed lower levels of STAT3 phosphorylation
- strong expression of cytoplasmic inactive STAT3 in NSCLC and malignant mesothelioma cases implies a major role for STAT3 in tumor motility, invasion, and metastasis via a nontranscriptional pathway
- Stat3alpha and Stat3beta have distinct intracellular dynamics, with Stat3beta exhibiting prolonged nuclear retention and reduced intranuclear mobility especially following ligand stimulation
- Ursolic acid is a novel blocker of STAT3 activation that may have a potential in prevention and treatment of multiple myeloma and other cancers.
- ATF2/STAT3 signaling pathways are activated and may play a role in development of eccrine porocarcinoma and eccrine poroma.
- PKCepsilon activation is essential for constitutive activation of Stat3 and prostate cancer progression.
- The IL-6/STAT3 antiapoptotic pathway is induced by short exposure to bile acid cocktail and low pH.
- IFNalpha is able to interfere with IL-6 signaling by inhibiting STAT3 activity and the abrogation of STAT3 activity accounts for the ability of IFNalpha to induce apoptosis in myeloma cells.
- Mutations in STAT3 underlie sporadic and dominant forms of the hyper-IgE syndrome. Eighteen discrete mutations, five of which were hot spots, were predicted to directly affect the DNA-binding and SRC homology 2 (SH2) domains.
- Together, these data demonstrate that NDRG2 expression in breast cancer cells is able to inhibit STAT3 activation via SOCS1 induction in a p38 MAPK dependent manner.
- low p-STAT3 in GCs may account for decreased fertilization, implantation, and pregnancy rates of in vitro fertilization in polycystic ovarian syndrome women
- CTR9 participates in the transcription of IL-6-responsive genes through the regulation of DNA association of STAT3 and modification of histone methylation
- In breast cancer stem-like cells, the STAT3 pathway was found to be positively regulated by mTOR signaling, whereas PTEN served as a negative regulator of both STAT3 and mTOR signaling.
- EGFR induces expression of IRF-1 via STAT1 and STAT3 activation leading to growth arrest of human cancer cells
- Observations suggest that suppression of Stat3 signaling may provide a potential therapeutic approach to overcoming DOX resistance in metastatic breast cancer cells.
- 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.
- define a second oncogenic pathway, STAT3 activation, which operates in activated B-cell-like Diffuse large B-cell lymphoma
- an IL-6-inducible STAT3 and CDK9 binding to the proximal gamma-FBG promoter as well as increased loading of RNA Pol II
- Thus the c-myc P2E behaves as a dual-purpose STAT3 element with anomalous characteristics in HepG2 cells.
- the potential mechanism by which cell-cell contact initiates STAT3 activation.
- human breast cells are a uniquely permissive environment for HGF transactivation by Src/Stat3 which may allow for the inappropriate activation of HGF transcription during the early stages of breast transformation
- We conclude that Stat3 binding is important for MASP2 promoter activity.
- Blocking Hsp90 disrupts IGF-I and IL-6-induced proangiogenic signaling cascades by targeting IGF-IR and STAT3 in pancreatic cancer
- Although this is a very rare case of HIV-1-integrated lymphoma, these data suggest that up-regulation of STAT3 caused by HIV-1 integration resulted in the development of B cell lymphoma in this special case.
- anti-apoptotic effects of STAT3 signaling in gastric cancer cells by enhancing Akt activation, Bad phosphorylation and Bcl-xL is mediated by REG Ialpha expression
- Reduced endometrial pSTAT3 and IL-11 may be involved in secretory transformation of glandular epithelium during receptivity. Reduced IL-11 production and STAT3 phosphorylation may contribute to unexplained infertility in some women.
- A model for binding of phosphopeptides to SH2 domain of STAT3 was presented.
- YC-1 inhibited Stat3 activity by enhancing the polyubiquitination of P-Stat3(705) induced by cisplatin.
- EGFR could activate the gp130/JAK/STAT3 pathway by means of IL-6 upregulation in primary human lung adenocarcinomas, making this pathway a potential target for cancer treatment.
- the astroglial differentiation effect of AICAR on neural stem cells was acting independently of AMPK and that the JAK-STAT3 pathway is essential for the gliogenic effect of AICAR.
- SN acts directly on neurons after hypoxia and ischemic insult to further their survival by activating the Jak2/Stat3 pathway.
- Regulates ATP-binding cassette transporter 3 (ABCA3) expression in vivo and in vitro.
- STAT3 mediates resistance to ATP depletion-induced apoptosis of proximal tubular epithelial cells, which may be a potential target in treatment of renal ischemic injury.
- Cooperative signaling through the signal transducer and activator of transcription 3 and nuclear factor-{kappa}B pathways in subtypes of diffuse large B-cell lymphoma
- variations in cell density can profoundly modify the extent of JAK-mediated persistent STAT3 phosphorylation; however, STAT3 activation was not sufficient to provide critical growth and survival signals in melanoma cell lines
- The Ang II/Rac1/STAT3 pathway is an important signaling pathway in the atrial myocardium to mediate atrial structural remodeling, and losartan and statin may be able to reverse Ang II-induced atrial structural remodeling in atrial fibrillation.
- a network involving signal coactivation of NF-kappaB and STAT3, differentially modified by p53 inactivation or mutation, promotes altered BAX/BCL-XL expression and cell survival in HNSCC.
- potential coordinative effects of Wnt, NF-kappaB and/or Stat3 activation on gastric cancer formation presumably by promoting the transcription of their common target genes.
- Abnormal STAT3 signalling in T cells from Sjogren's syndrome patients.
- Sp1 recruits ATF3, c-Jun, and STAT3 to obtain the requisite synergistic effect in neuronal injury through DINE neuronal injury-inducible gene
- Interferon gamma induces XAF1 and Noxa expression and potentiates apoptosis by STAT3 activation
- autoregulation of DeltaNp63 gene transcription is mediated through activation of STAT3 and its subsequent binding to the STAT3RE.
- Results suggest that STAT3 siRNA can inhibit the invasion ability of colon cancer cells through inducing anoikis, which antiapoptotic genes survivin and Bcl-xL contribute to regulation of anoikis.
- LMP1 stimulated STAT3 Tyr 705-dependent nuclear accumulation, as well as the phosphorylation of STAT3 at both Tyr 705 and Ser 727.
- identify leptin/STAT3 signaling as a novel pathway for survivin expression in breast cancer cells
- an essential role of the SH2B1 variants in the activation of the Src kinase and the resulting mitogenic response--extending to phenotypic cell transformation and involving the established Src substrate STAT3.
- HOXA1 partially mediates oncogenic transformation of the immortalized human mammary epithelial cell through modulation of the STAT3 and STAT5B pathways.
- pSTAT3 is a potential biomarker of melanocytic transformation and progression
- Nuclear accumulation of STAT3 activation by IL-6 plays a key role in iNOS expression and resultant DNA damage, leading to EBV-mediated Naso-Pharyngeal Carcinoma(NPC).
- Novel mitogenic signaling pathway in airway smooth muscle cells leading from PDGF to Stat3 and cell cycle gene regulation.
- Theses findings illustrate the biologic significance of JAK1, 2/STAT3 signaling in colorectal cancer (CRC) progression and provide novel evidence that the JAK/STAT3 pathway may be a new potential target for therapy of CRC.
- 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
- STAT3, Twist, and AKT2 form a functional signaling axis to regulate pivotal oncogenic properties of cancer cells
- STAT3 activation functionally mimicked IL-21 treatment and that STAT3-mediated BLIMP1 up-regulation occurred despite high BCL6 expression levels
- STAT3 activation is independent of the EGFR/MEK/ERK signaling pathway
- STAT3 activation mediates COX-2 expression and ischemic tolerance.
- Src-dependent STAT-3-mediated VEGF expression is a major mechanism of 14,15-EET-induced angiogenesis
- HER2-dependent transcriptional upregulation and protein secretion of MMP-7 are mediated by activated STAT3.
- The C-28 methyl ester of the oleane triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO-Me) inhibits activation of the JAK1-->STAT3 pathway by forming adducts with both JAK1 and STAT3.
- STAT3 enhances invasiveness of tumours and trophoblast cells.
- PIM1 kinase plays a critical role in the STAT3 --> PIM1 --> NFkappaB stress response pathway
- Single nucleotide polymorphism in STAT3 gene is associated with ulcerative colitis
- HA binding to tumor cells promotes Nanog protein association with CD44 followed by Nanog activation and the expression of pluripotent stem cell regulators, and forms a complex with Stat-3 in the nucleus leading to Stat-3 and MDR1 activation
- Rapid activation of Stat3 and ERK1/2 by nicotine modulates cell proliferation in human bladder cancer cells.
- lower levels of pSTAT3 were found in the nuclei of hepatitis E virus ORF3-expressing Huh7 human hepatoma cells stimulated with EGF. This results in downregulation of the acute-phase response, a major determinant of inflammation in the host.
- Results do not support a major role for STAT3 variants in BMI, obesity and insulin resistance in an adult male population.
- The Stat3-activating Tyk2 V678F mutant does not up-regulate signaling through the type I interferon receptor but confers ligand hypersensitivity to a homodimeric receptor
- Mutations are implicated in hyper-IgE syndrome.
- Epigallocatechin-3-gallate suppresses the pathological characteristics of keloids through inhibition of the STAT3-signaling pathway.
- These results indicate that the IL-6 family of cytokines modulates STAT3 activation by desumoylation and inactivation PML through SENP1 induction.
- Stat3 is involved in metastatic behavior of human prostate cancer cells and may provide a therapeutic target to prevent metastatic spread of primary prostate cancer.
- persistent activation of STAT1, STAT3, and STAT5 correlate with resistance to vorinostat in lymphoma cell lines
- nuclear STAT3 expression is associated with poor patient prognosis in the intestinal subtype
- a critical role for a EGF-R-connected p60c-src-kinase-mediated pathway involving STAT3 and contributing to cell survival and proliferation within colorectal carcinomatumours.
- Y14 interacts with STAT3 and regulates the transcriptional activation of STAT3 by influencing the tyrosine-phosphorylation of STAT3.
- KLF11 may interfere with glucose homeostasis in a Danish general population and that STAT3-mediated up-regulation of KLF11 transcription was impaired by the -1659G>C variant.
- Down-regulating signal transducer and activator of transcription 3 (STAT3) expression by short hairpin RNA in Smad4-deficient cells prevented TGFbeta-induced invasion
- Platelet-derived growth factor-induced cell growth, migration, and IL8 secretion in corneal fibroblast involve the JAK2-STAT3 signaling pathway.
- This study uncovers a novel link between STAT3 and interleukin 8, the deregulation of which plays a key role in the malignant behavior of glioblastoma cells.
- In addition, STAT3 knockdown inhibited anchorage-independent growth and induced apoptosis in CAOV3 cells, and decreased tumor growth in nude mice implanted with ovarian cancer cells.
- Overexpression of phosphorylated-ATF2 and STAT3 in cutaneous squamous cell carcinoma, Bowen's disease and basal cell carcinoma.
- parvovirus B19 NS1 protein modulates inflammatory signaling by activation of STAT3/PIAS3 in human endothelial cells
- There is a marked increase in STAT3 activation in many forms of glomerulonephritis. The correlation of STAT3 activation with clinical and histologic parameters suggests that this pathway plays an important role in the pathogenesis of kidney disease.
- IL-6 treatment induced MUC4 expression through the gp130/STAT3 pathway, indicating the direct role of IL-6 on the activation of the intestinal mucin gene MUC4 in gastric cancer cells
- nonoverlapping, sequential activation of STAT3 and STAT5 selects for multilog expansion, programming, and dendritic cell DC1 polarization of tumor-competent DCs from CD34(pos) cells
- Data show that platelet-derived growth factor-BB induces mesenchymal stem cell proliferation via activation of the Jak2-Stat3 transcription cascade.
- a failure of CD4+ T cells harboring heterozygous STAT3 mutations to generate interleukin 17-secreting cells due to a failure to express sufficient levels of the Th17-specific transcriptional regulator retinoid-related orphan receptor t.
- IL-12Rbeta1- and STAT-3--dependent signals play a key role in the differentiation and/or expansion of human IL-17-producing T cell populations in vivo.
- The importance of STAT3 signaling in maintenance and survival of medulloblastoma cells.
- heterozygous STAT3 mutations were identified in 34 of 35 unrelated Hyper-IgE syndrome families; patients had impaired T(H)17 cell development, and those with SH2 domain mutations had reduced STAT3 phosphorylation
- results suggest that STAT3 is a target of beta-catenin/TCF pathway and might participate in esophageal tumorigenesis
- These findings show a novel mode by which HIF-1alpha is regulated not only in cancer cells but also in the tumor-associated inflammatory cells, suggesting Stat3 as an important molecular target for inhibiting the oncogenic potential of HIF-1.
- Data show that Stat3 activation and its interaction with Ec-gp96, which in turn interacts with E. coli outer membrane protein A, are critical for E. coli invasion.
- the loss of PIAS3 in glioblastoma multiforme contributes to enhanced STAT-3 transcriptional activity and subsequent cell proliferation
- the Th2 cytokine IL-21 is abnormally expressed in Hodgkin lymphoma cells, which regulates STAT3 signaling and attracts Treg cells via regulation of MIP-3alpha
- Significant p-STAT3 expression is associated with colorectal adenocarcinoma.
- overexpression of p-ATF2, p-STAT3 and possibly p53, but not p63 or p73, may contribute to the tumorigenesis of cutaneous vascular tumors.
- Wnt (Wnt2), Stat3, and Notch-1 and -2 signaling are correlated in human epidermal tumors.
- Enhanced STAT3 signaling responsiveness to proinflammatory factors may impact on mechanisms of muscle repair and regeneration.
- Plays a role in the pathogenesis of gestational trophoblastic disease, probably through the regulation of apoptosis.
- Co-stimulation of G(s) and G(q) can result in the fine-tuning of STAT3 activation status, and this may provide the basis for cell type-specific responses following activation of hIP.
- Two cases of hyperactivated STAT3 in ALK-positive diffuse large B-cell lymphoma with clathrin-ALK fusion are reported.
- High expression and activation of STAT3 exist in laryngeal carcinomas.
- STAT3 expression was significantly related to overall 5-year survival rate in breast cancer patients.
- This review summarizes the current understanding of the roles of STAT3 in IBD and the potential of targeting STAT3 for the treatment of IBD, emphasizing recent observations [review]
- STAT3 activation and nuclear accumulation in response to Hepatocyte Growth Factor requires nuclear-proximal activated c-Met.
- STAT3 NH(2)-terminal domain plays an important role in the interleukin-6 signaling pathway by interacting with the p300 bromodomain, thereby stabilizing enhanceosome assembly.
- Our study suggests a potential role of the STAT3 polymorphisms and their haplotypes in susceptibility to NAFLD and disease severity.
- STAT3 constitutive activation, alone and in concurrence with EGFR expression, plays an important role in high-grade/malignant gliomas and targeting STAT3/JAK2 sensitizes these tumors to anti-EGFR and alkylating agents
- S727 phosphorylation is sufficient to activate Stat3, thereby driving prostate tumorigenesis independent of Y705 phosphorylation.
- BDNF- and seizure-dependent phosphorylation of STAT3 cause the adenosine 3',5'-monophosphate (cAMP) response element-binding protein (CREB) family member ICER (inducible cAMP early repressor) to bind with phosphorylated CREB at the Gabra1:CRE site.
- elevated Stat3 phosphorylation in 19 of 100 (19%) bladder cancer tissues as well as bladder cancer cell lines, WH, UMUC-3 and 253J.
- TCPTP is a negative regulator of SFK, JAK1 and STAT3 signalling during the cell cycle.
- Results suggest that STAT3 decreases the pVHL-mediated ubiquitination of HIF-1alpha through competition with pVHL for binding to HIF-1 alpha, and then stabilizes HIF-1alpha protein levels.
- IL11 inhibits human extravillous trophoblast invasion via STAT3, indicating a likely role for IL11 in the decidual restraint of EVT invasion during normal pregnancy.
- These results support the hypothesis that STAT3 and CREB play an important role in leptin signaling pathway that leads to the proliferation of Ishikawa cells, thus establishing a direct association between obesity and endometrial tumorogenesis.
- S-glutathionylation of STAT3, a modification that may exert regulatory function in STAT3 signaling.
- data indicate overexpression of mesothelin in pancreatic cancer cells leads to constitutive activation of Stat3, resulting in enhanced expression of cyclin E & cyclin E/cyclin-dependent kinase 2 complex formation & increased G(1)-S transition
- guggulsterone not only induces apoptosis, but also inhibits angiogenesis and metastasis in colon cancer cells by blocking STAT3 and VEGF expression
- EBNA2 is a transcriptional coactivator of STAT3 by influencing its DNA-binding activity.
- Cell confluency-induced Stat3 activation regulates NHE3 expression by recruiting Sp1 and Sp3 to the proximal NHE3 promoter region during epithelial dome formation.
- There are associations with JAK2 and STAT3 implicating the role of this signaling pathway in inflammatory bowel disease.
- Activated STAT3 is a required part of the continuous activation of B3/B4 genes, which protects tumor cells from dying.
- In primary human leukemia samples, there was a positive correlation between HMGA1a and STAT3 mRNA. Moreover, blocking STAT3 function in human leukemia or lymphoma cells led to decreased cellular motility and foci formation.
- Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1).(
- Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial-mesenchymal transition in ovarian carcinomas.
- In this review, studies of STAT3 deficiency in humans highlight nonredundant roles of STAT3 in diverse cellular processes such as antimicrobial immunity and protection at epithelial barriers, and in hyper-IgE syndrome.
- STAT3 analysis of essential thrombocythemia shows that in about half of patients, STAT3 hyperactivation is independent of JAK2 mutations. The hyperactivation of STAT3 by JAK2 mutations or promoter activation may be a critical step in development of ET.
- These results indicate that HDAC3 may act as a scaffold protein for PP2A to regulate the LIF/STAT3-mediated signaling pathway.
- Boswellic acid is a novel inhibitor of STAT3 activation and has potential in the treatment of cancer.
- Interaction between STAT3 and Fer was observed in all prostate cancer cell lines tested, and this interaction is modulated by interleukin-6.
- Results indicate that H. pylori CagA activates the STAT3 signaling pathway in vitro and in vivo, providing a potential mechanism by which chronic H. pylori infection promotes the development of gastric cancer.
- there was a statistically significant dependence of the EGFR status on STAT3 expression in neoplastic tissues
- BITC (benzyl isothiocyanata) induces apoptosis in some types of pancreatic cancer cells by inhibiting the STAT-3 signaling pathway.
- Sustained Src inhibition results in signal transducer and activator of transcription 3 (STAT3) activation and cancer cell survival via altered Janus-activated kinase-STAT3 binding.