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Validated All-in-One™ qPCR Primer for STAT5B(NM_012448.3) Search again
Product ID:
HQP017774
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GHISID2, STAT5
Gene Description:
signal transducer and activator of transcription 5B
Target Gene Accession:
NM_012448.3(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 family of transcription factors. 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 mediates the signal transduction triggered by various cell ligands, such as IL2, IL4, CSF1, and different growth hormones. It has been shown to be involved in diverse biological processes, such as TCR signaling, apoptosis, adult mammary gland development, and sexual dimorphism of liver gene expression. This gene was found to fuse to retinoic acid receptor-alpha (RARA) gene in a small subset of acute promyelocytic leukemias (APLL). The dysregulation of the signaling pathways mediated by this protein may be the cause of the APLL.
Gene References into function
- The data presented here demonstrate that, in contrast to activation by the cytokine, growth hormone (GH), the activation of STAT5b by the growth factor, epidermal growth factor (EGF), requires overexpression of the EGF receptor (EGFR).
- STAT5 isoform expression, GM-CSF-induced STAT5 activation, and STAT5 target-gene expression are altered significantly during monocyte/macrophage differentiation
- increase in Cyclin D1 promoter activity is predominantly mediated by the Jak2/Stat5 signaling pathway. PRL induces Stat5a and 5b to bind to Cyclin D1 promoter
- Interactions of STAT5b-RARalpha, a novel acute promyelocytic leukemia fusion protein, with STAT3 and STAT5 signaling pathways.
- Oligomerization of the coiled-coil domain of Stat5 in the Stat5-RARalpha fusion protein leads to stable binding of the corepressor SMRT and is accompanied by an impaired response to differentiation signals in hematopoietic cell
- Up-regulation of RFC2 and the kinase pim-1 by BCR/ABL requires activation of STAT5b by signaling from SH3+SH2 domains of BCR/ABL.
- Our study thus suggests a functional cooperation between AR and Stat5.
- No evidence was found for STAT5b rearrangement at the chromosomal or molecular levels in primary leukemias. STAT5 activation is probably a secondary event in most leukemias.
- CPAP was found to augment Stat5-mediated transcription.
- Signal transducer and activator of transcription (Stat)5a and Stat5b are critical for normal immune function.
- role in mediating synergism between c-src and epidermal growth factor receptor
- role in suppressing transcriptional activity of estrogen receptors and inducing apoptosis in breast cancer cells
- Role of c-Jun-N-terminal kinase and signal transducer and activator of transcription 5 in regulation of eosinophil apoptosis by nitric oxide.
- Stat5 plays an important role in IFN-signaling and participates in the induction of Type I IFN-dependent responses.
- In tissues from 33 individuals with head and neck cancer, Stat5 activation levels were correlated with progression to a malignant phenotype.
- Mpl-L-treated Stat5b-deficient mice demonstrated significantly delayed hematopoietic recovery, while Stat5b-deficient mice did not
- diminished N-domain-mediated oligomerization affected transcriptional activation by both Stat1 and Stat5a/b in a promoter-specific manner.
- Crossing the STAT5b constitutively active transgene onto the IL-7 receptor-deficient background restores immature B and mature B cell populations as seen by significant increases of immature B and mature B cells.
- Stat5B is activated by pathways involving FGFR3 and Pyk2
- Perturbation of STAT5a&b expression by addition of ODNs decreased proliferative potential of the CML and the AML blasts as well as enhanced their apoptosis
- requisite role of the Jak2/Stat5B pathway in mediating episodic growth hormone regulation of CYP2C11
- Stat5 activation results in the induction of pax5 and bcl-xL in early thymic lymphoid progenitor cells and thereby redirects these cells down the B cell lineage.
- Study shows that active Stat5 distinguished prostate cancer patients whose disease is likely to progress earlier; therefore, active Stat5 may be a useful marker for selection of more individualized treatment.
- STAT5b may mediate the transcriptional activation of cyclin D1 after hypoxic stimulation.
- IFNalpha induces the activation of STAT5 in melanoma cells, and in STAT5-overexpressing cells, this contributes to IFNalpha resistance.
- Stat5b A630P mutant is an inactive transcription factor by virtue of its aberrant folding and diminished solubility triggered by a misfolded SH2 domain.
- STAT5b is an inefficient signal transducer and transcription factor, the detrimental impact on signaling pathways important for normal growth and immunity explains, in part, the complex clinical phenotype of GH insensitivity and immune dysfunction
- STAT5A and STAT5B may play significant roles in the growth and the process of apoptosis of selected human cutaneous T-cell lymphoma cells.
- STAT5b and HNF4alpha exhibit bi-directional cross-talk that may augment HNF4alpha-dependent gene transcription while inhibiting STAT5b transcriptional activity via the inhibitory effects of HNF4alpha on JAK2 phosphorylation
- STAT5 is a direct binding partner to EGFR and ErbB4.
- Cytoskeleton plays an important role in STAT5 activation and translocation into the nucleus in MCF7 cells stimulated with EGF.
- STAT5b activity in breast cancer cells is modulated by various mutations of tyrosines within the transactivation domain.
- Data show that STAT5 binds in vivo to the NCAM2 intron in the NKL natural killer cell line and that this binding is induced by cytokines that activate STAT5.
- Transgenic constitutively activated STAT5b-CA naive CD4+ T cells display a 4-fold greater expression of IL-15 receptor alpha chain on their surface when compared with wild-type T cells.
- STAT5b propagates an important IL-2-mediated signal for the in vivo accumulation of functional regulatory T cells
- Therapeutic activation of the GH:STAT5b axis therefore represents a novel target for restoring both normal anabolic metabolism and mucosal tolerance in CD.
- Defective STAT5b is an etiology for IGF deficiency and the growth hormone insensitivity phenotype.
- ability of prolactin to activate Stat5 and activating protein-1 was inversely related in mammary cell lines
- in addition to growth arrest and induced differentiation, OSM also sensitizes normal and transformed osteoblasts to apoptosis by a mechanism implicating (i) activation and nuclear translocation of STAT5 and p53 and (ii) an increased Bax/Bcl-2 ratio
- IGF-1 expression is activated by hypoxia through STAT5b in human HepG2 cells
- STAT5 expression is required for the maintenance and expansion of primitive hematopoietic stem and progenitor cells, both in normal as well as leukemic hematopoiesis.
- STAT5 protein could contribute to the progression and proliferation of intraductal papillary mucinous neoplasms.
- the phosphorylation of Tyr(1077) on LepRb during receptor activation, substantiate the hypothalamic regulation of STAT5 and S6 by leptin, and define the alternate LepRb signaling pathways
- Here, we demonstrate for the first time that EGF stimulation enhances S731 phosphorylation.
- phosphorylated STAT5 could be the most meaningful test for rapidly identifying patients who may respond to flt3 or other tyrosine kinase inhibitors
- Brk can directly phosphorylate STAT5b on Y699. Subsequently, this Brk-mediated STAT5b phosphorylation leads to STAT5b transcriptional activity, and this activity is further increased by kinase active c-Src.
- The work presented here provides the first evidence of synergy between AR and the prolactin signaling protein Stat5a/b in human prostate cancer cells.
- By using a Thr757/Val mutant of STAT5 we also demonstrate that the 757 serine/threonine conserved residue, which is in the STAT5A region involved in the interaction with LMW-PTP, is essential for such an association
- HOXA1 partially mediates oncogenic transformation of the immortalized human mammary epithelial cell through modulation of the STAT3 and STAT5B pathways.
- the phosphorylation status of STAT5 of Hodgkin and Reed-Sternberg cells in cHL could be a prognostic marker in HL.
- murine OSMR initiates STAT5 activation directly via the receptor bound Janus kinases. Intriguingly, the murine receptor preferentially recruits JAK2, whereas the human receptor seems to have a higher affinity for JAK1.
- These studies demonstrate positive cross talk between ER, c-Src, EGFR, and STAT5b in ER+ breast cancer cells.
- An IL-2-STAT5 signaling axis is involved in the expression of IL-10 by human regulatory T cells, an axis that is regulated by the STAT-responsive element within intron 4 and epigenetic modification of this element.
- The enhanced SULT1E1 activity may have a role in inhibiting GH-stimulated STAT5b phosphorylation and IGF-1 synthesis via the sulfation and inactivation of E2.
- Circulating angiogenic cells in diabetic angiopaathy is a multistage process requiring sequential activation of transcriptional factors, including STAT5 and PPARG.
- constitutive STAT5 signaling enhances tumor growth, invasion, and epithelial-to-mesenchymal transition in squamous epithelial carcinogenesis