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Validated All-in-One™ qPCR Primer for STAT5A(NM_003152.3) Search again
Product ID:
HQP017771
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MGF, STAT5
Gene Description:
signal transducer and activator of transcription 5A
Target Gene Accession:
NM_003152.3(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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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 is activated by, and mediates the responses of many cell ligands, such as IL2, IL3, IL7 GM-CSF, erythropoietin, thrombopoietin, and different growth hormones. Activation of this protein in myeloma and lymphoma associated with a TEL/JAK2 gene fusion is independent of cell stimulus and has been shown to be essential for the tumorigenesis.
Gene References into function
- Jak-Stat and PI 3-kinase activation pathways regulate the TPO-induced survival of megakaryocytic cells via Bcl-xL gene expression.
- To examine the roles of BCR/ABL-activated individual signaling molecules we inducibly expressed a dominant negative (DN) form of Ras, phosphatidylinositol 3-kinase, and STAT5 alone or in combination in p210 BCR/ABL-positive K562 cells.
- substrates for calpain in in platelets[stat5protease]
- 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
- constitutive activation of Stat5a may contribute to head and neck cancer cell proliferation.
- Prostaglandin-E2 enhances EPO-mediated STAT5 transcriptional activity by serine phosphorylation of CREB.
- CPAP was found to augment Stat5-mediated transcription
- NF-kappaB is recruited directly to the promoters of several target genes, including STAT5a
- Signal transducer and activator of transcription (Stat)5a and Stat5b are critical for normal immune function.
- role during eosinophil differentiation using umbilical cord blood-derived CD34(+) 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.
- STAT5, in concert with the glucocorticoid receptor, recruits a multifunctional coactivator complex to initiate the PRL-dependent transcription
- Stat5-mediated gene transcription requires binding of the coactivator of transcription CBP
- We show that the association of STAT5 and LMW-PTP does not exclusively involve the phosphatase active site and phosphotyrosine residue of STAT5.
- Stat5a was nuclear localized and tyrosine phosphorylated in 59 of 78 (76%) breast cancers examined; 38 of 78 (49%) demonstrated Stat5a nuclear localization in more than 25% of the breast cancer cells within the adenocarcinomas.
- In advanced arteriosclerotic lesions, the activation of the Tie2-mediated STAT5 signaling pathway may negatively regulate vessel growth.
- diminished N-domain-mediated oligomerization affected transcriptional activation by both Stat1 and Stat5a/b in a promoter-specific manner.
- IL-7 induced the death of DN STAT5 expressing 697 cells occurs through caspase-dependent and -independent mechanisms that both require mitochondrial activation.
- 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
- Stat5 activity in human breast cancer correlates with favorable prognosis
- Aberrant regulation of STAT5 has been observed in solid tumors as well as in patients with either chronic or acute myeloid leukemia [review].
- STAT5A has a role in human hematopoietic stem and progenitor cell self-renewal and diverts differentiation to the erythroid lineage
- STAT5 is involved in cytokine-mediated up-regulation of MIST gene expression.
- nuclear localization of STAT5A and stimulation of the beta-casein promoter requires nuclear translocation of the ERBB4 intracellular domain 4ICD; binding of the two proteins at transcription factor target promoters results in activation of gene expressio
- an invasion-suppressive role of Stat5 in human breast cancer
- STAP-2/BKS is a modulator of STAT5-mediated signaling
- These data suggest that Stat5 tetramers are associated with leukemogenesis.
- 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.
- Consistently, overexpression of a constitutive active STAT5A leads to anchorage-independent cell cycle progression. Therefore, integrin-dependent STAT5A activation controls IL-3-mediated proliferation.
- 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.
- The absence of STAT 5a in the abnormal breast epithelial cells may indicate a defect contributory to the abnormal state.
- Constitutive activation of Stat5A is associated with oral squamous cell carcinoma
- Results suggest that the antiapoptotic effects of erythropoietin in neuronal cells require the combinatorial activation of multiple signaling pathways, including STAT5, AKT, and potentially MAP kinase.
- down-modulation of C/EBPalpha is a prerequisite for STAT5-induced effects on self-renewal and myelopoiesis in human cord blood-derived stem/progenitor cells
- STAT5A and STAT5B may play significant roles in the growth and the process of apoptosis of selected human cutaneous T-cell lymphoma cells.
- STAT5 activation specifically cooperates with the loss of p53 function in B-cell lymphomagenesis
- Effect of signal transducer and activator of transcription 5 proteins on indomethacin-induced cell division inhibition in chronic myelogenous leukemia cells.
- In polycythemia vera JAK2(V617F) may induce endogenous erythroid colonies via the STAT5/Bcl-xL pathway.
- STAT5 is a direct binding partner to EGFR and ErbB4.
- STAT5 has a role in steroid-resistant ulcerative colitis
- 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.
- Expression of Stat5 is helpful in selecting patients who may benefit from endocrine therapy in breast cancer.
- a negative cross talk between PR and Stat5a/GR may contribute to the physiological role of progesterone to repress lactogenic hormone induction of the beta-casein gene
- 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
- constitutively active Stat5 mutant forms a complex with the p85 subunit of phosphatidylinositol 3-kinase and the scaffolding adapter Gab2 in leukemic bone marrow cells, resulting in the activation of Akt/PKB, a crucial downstream target of PI3-K
- inhibition of ITD/Flt3 activity did not prevent the phosphorylation of ERK, STAT5 or Akt in some primary AML cells. In parallel, in these cells, Flt3 and ERK or Akt cooperate to regulate cell survival
- VEGF-A, STAT5 and AKT are downregulated in acute myeloid leukemia blasts of patients treated with SU5416
- Found in in situ lesions. May play some role in the prognosis/invasion of extramammary Paget's disease.
- Stat5 activation enhanced SMN2 promoter activity with increase in both full-length and deletion exon 7 SMN transcripts.
- There is a major role for STAT5a in the differentiation of keratinocytes, where it contributes to involucrin expression by activating the PPARgamma signal.
- constitutively activated naturally occurring STAT5 Delta present in the leukocytes of most HIV-positive individuals acts as a negative regulator of HIV expression.(STAT5 DELTA)
- 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.
- ability of prolactin to activate Stat5 and activating protein-1 was inversely related in mammary cell lines
- analysis of STAT5, CIS, and SOCS2 interactions with the growth hormone receptor
- 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
- after tyrosine phosphorylation, STAT5a accumulates in the nucleus because of its retention by DNA binding
- Mutations occur in Reed Sternberg cells and nuclear phospho-STAT5 accumulates in the cell nucleus.
- Myc down-regulation is a mechanism to activate the Rb pathway in STAT5A-induced senescence
- Acts as a key tumor suppressor by reciprocally inhibiting expression of oncogenic nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) in T-cell anaplastic large cell lymphomas.
- 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.
- IL-2 selectively enhanced production of IL-10 in HOZOT primarily through activation of STAT5, which synergistically acts with NF-kappaB/NFAT activation, implying a novel regulatory mechanism of IL-10 production in Treg cells.
- The SRC-STAT5 pathway is essential for decidualization of estrogen-primed human endometrial stromal cells.
- The work presented here provides the first evidence of synergy between AR and the prolactin signaling protein Stat5a/b in human prostate cancer cells.
- activation of STAT5 sustains FOXP3 expression in both Treg and Teff cells and contribute to our understanding of how cytokines affect the expression of FOXP3
- signal transducer and activator of transcription 5A and Jak2 co-overexpression cooperatively reverses epithelial-mesenchymal transition and promotes differentiation in human breast cancer cells
- STAT5 and nuclear factor-kappaB pathways collaborate in HL genesis
- STAT5A and progesterone receptor are coordinately recruited to a distal enhancer of 11beta-HSD2 gene.
- STAT5 downregulation in CD34+ cells promotes megakaryocytic development, whereas activation of STAT5 drives erythropoiesis
- IL-3-mediated cell expansion and arterial morphogenesis rely on STAT5 activation
- persistent activation of STAT1, STAT3, and STAT5 correlate with resistance to vorinostat in lymphoma cell lines
- Homoharringtonine affects the JAK2-STAT5 signal pathway through alteration of protein tyrosine kinase phosphorylation in acute myeloid leukemia cells
- Induction of STAT5A activity in CD34(+) cells resulted in impaired myelopoiesis and induction of erythropoiesis, which was most pronounced at the highest STAT5A transactivation levels.
- SHD1 is a novel cytokine-inducible negative feedback regulator of STAT5a.