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anti-Human STAT5A Antibodies:
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Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177246
Johnston, Choi, Diamond, Yang, Crotty: STAT5 is a potent negative regulator of TFH cell differentiation. in The Journal of experimental medicine 2012
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Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177254
Bromberg, Darnell: The role of STATs in transcriptional control and their impact on cellular function. in Oncogene 2000
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Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177247
Riou, Yassine-Diab, Van grevenynghe, Somogyi, Greller, Gagnon, Gimmig, Wilkinson, Shi, Cameron, Campos-Gonzalez, Balderas, Kelvin, Sekaly, Haddad: Convergence of TCR and cytokine signaling leads to FOXO3a phosphorylation and drives the survival of CD4+ central memory T cells. in The Journal of experimental medicine 2007
Show all 4 Pubmed References
Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177248
Gouilleux, Wakao, Mundt, Groner: Prolactin induces phosphorylation of Tyr694 of Stat5 (MGF), a prerequisite for DNA binding and induction of transcription. in The EMBO journal 1994
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Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177249
Imada, Leonard: The Jak-STAT pathway. in Molecular immunology 2000
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Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177250
Liu, Gaffen, Goldsmith: JAK/STAT signaling by cytokine receptors. in Current opinion in immunology 1998
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Human Monoclonal STAT5A Primary Antibody for ICS - ABIN1177255
Van De Wiele, Marino, Murray, Vo, Whetsell, Teague: Thymocytes between the beta-selection and positive selection checkpoints are nonresponsive to IL-7 as assessed by STAT-5 phosphorylation. in Journal of immunology (Baltimore, Md. : 1950) 2004
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Human Polyclonal STAT5A Primary Antibody for IHC - ABIN967098
Dentelli, Del Sorbo, Rosso, Molinar, Garbarino, Camussi, Pegoraro, Brizzi: Human IL-3 stimulates endothelial cell motility and promotes in vivo new vessel formation. in Journal of immunology (Baltimore, Md. : 1950) 1999
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Human Polyclonal STAT5A Primary Antibody for IHC - ABIN967097
Meinke, Barahmand-Pour, Wöhrl, Stoiber, Decker: Activation of different Stat5 isoforms contributes to cell-type-restricted signaling in response to interferons. in Molecular and cellular biology 1997
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HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis.
Data show that knockdown of STAT transcription factors STAT3 and/or STAT5 reduces DNA methylcytosine dioxygenase Ten-eleven translocation 1 (TET1) level.
the two cell lines exhibited relatively low protein expression levels of p53, lower levels of p53 and TPp53BP1 transcripts were detected in the K562/G cells. Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 pathway
Peripheral blood Tregs failed to effectively utilize IL-2 and had relatively little STAT5 phosphorylation in active ankylosing spondylitis.
These results indicate that IL-3 regulates endothelial cells-extracellular vesicles release, cargo and IL-3 angiogenic paracrine action via STAT5.
Our finding supports that STAT3 was the potential treated target for breast cancer therapy, whereas STAT5A/5B/6 were potential prognostic markers for better survival of BC, providing more accurate prognosis.
Similar to normal developmental programs, oncogenic functions of STAT5 rely on molecular crosstalk with PI3K/AKT signaling for the initiation, and in some instances the progression, of breast cancer. (Review)
As targets of oncogenes with intrinsic tyrosine kinase activity, STAT3 and STAT5 become constitutively active in hematologic neoplasms and solid tumors, promoting cell proliferation and survival and modulating redox homeostasis via regulation xCT expression. (Review)
we demonstrated that Imatinib mesylate (IM)impaired T cell survival through the inhibition of IL-7 and STAT5-p but not TCR signaling which remained unaffected during IM therapy. Thus, off-target inhibitory effects of IM on IL-7 and STAT5-p explain how T cell lymphopenia occurs in patients treated with IM.
Our results suggest the regulation of STAT5A via epigenetic mechanisms during normal pregnancy and the association of STAT5A epigenetic dysregulation in pregnancy related complications
dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5, JAK2, and STAT3 and downstream molecules including p-CrkL, Mcl-1, Bcl-XL, and Bcl-2 proteins in K562 cells.
Two p53 binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 responsiveness in a luciferase reporter gene.
STAT3/miR-211/STAT5A signaling plays a key role in mesenchymal stem cell migration.
Stat5 activation increased the DNA binding activity of NF-kappaB though binding of p-Stat5 and p-RelA in nucleus.
these data suggest that ROCK2 signaling plays a critical role in controlling the development of TFH cells induced by autoimmune conditions through reciprocal regulation of STAT3 and STAT5 activation.
This is the first report of a survival disadvantage of EBV+ patients with CLL, and the first time that STAT5b expression is correlated with survival. The correlation of STAT5 expression with the presence of the virus, along with our survival correlations defines a subgroup of patients with CLL that may benefit from anti-STAT agents.
STAT5 signaling axis drives abnormal cell proliferation in autosomal dominant polycystic kidney disease.
O-GlcNAcylation and tyrosine phosphorylation act together to trigger pYSTAT5 levels and oncogenic transcription in neoplastic cells. A mutated hyperactive gain-of-function (GOF) STAT5 without O-GlcNAcylation resulted in decreased tyrosine phosphorylation, oligomerization and transactivation potential and complete loss of oncogenic transformation capacity.
STAT5 interacted with minichromosome maintenance (MCM) complex, suggesting that STAT5 directly facilitates viral DNA replication by recruiting the helicase complex of the cellular DNA replication machinery to viral DNA replication centers.
High STAT5 phosphorylation is associated with systemic lupus erythematosus.
E2F3 transcription factor variant impairs STAT5 signaling and mammary gland remodeling during pregnancy in mice
NK cell numbers are decreased in Stat5a-Stat5b tetramer-deficient double knockin mice, but the mechanism was not investigated. Here we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-associated genes.
endogenous growth hormone induces UCP1 expression in adipose tissue via STAT5
Each mutation decreased STAT5 binding and altered IL-2-induced Il2ra gene expression, revealing that individual elements within the superenhancer were not functionally redundant and that all were required for normal gene expression.
findings indicate that STAT5 contributes to the remarkable IL-3-mediated inhibition of RANKL-induced osteoclastogenesis by activating Id genes and their associated pathways.
Results suggest activation of H2AX via promoter demethylation in specific populations of basal mammary cells that is induced by a signal from neighboring luminal cells with hyper STAT5 activity.
On the basis of our ChIP data and these previous findings, we hypothesize that PDC may modulate STAT5's ability to regulate gene expression by controlling histone or STAT5 acetylation
STAT5 gene deletion had a minor effect on cholesterol metabolism, as evidenced by no changes in expression of cholesterol transport and cholesterol synthesis genes, and numeric changes in serum and liver cholesterol levels. These minor changes in cholesterol metabolism may not have been sufficient to influence on cholesterol crystal and gallstone formation in lithogenic diet-fed STAT5 LKO mice.
Stat5 deficiency has a strong impact upon transcriptional heterogeneity in single sorted c-Kit+Lin-Sca-1+ (KLS) cells or CD150+CD48- KLS long-term repopulating hematopoietic stem cells.
mice carrying Stat5a/b inactivation specifically in kisspeptin cells were generated. These mutants exhibited an early onset of estrous cyclicity, indicating that STAT5 transcription factors exert an inhibitory effect on the timing of puberty.
Upon deletion of the STAT5 response elements from the Socs2 promoter in mice, cytokine induction was abrogated, while basal activity remained intact. Our data suggest that promoter-bound STAT5 modulates cytokine responses and enhancer-bound STAT5 is mandatory for gene activation.
Instead, we find that STAT5B is dominant over STAT5A in CD4(+) 'helper' T cells for both effector and regulatory (Treg) responses and, therefore, uniquely necessary for immunological tolerance.
Data indicate that obesity-induced insulin resistance and lipotoxicity can be treated with ginsenoside Rg3, which acts though the STAT5-PPAR gamma pathway in vivo and in vitro.
STAT5a regulates miR-135a transcription by binding to both miR-135a-1 and miR135a-2 promoter elements
These studies establish the importance of STAT5 in macrophages during ductal morphogenesis in the mammary gland and demonstrate that altering STAT5 function in macrophages can affect the development of tissue-specific disease.
findings show that Stat5 is required for CD103(+) dendritic cell and alveolar macrophage development.These findings demonstrate the critical importance of Stat5 signaling in maintaining lung homeostasis, and underscore the importance of resident macrophages in moderating tissue damage and excess inflammation.
STAT5 target genes such as Oncostatin M were highly expressed in FLT3-ITD(+) myeloid but not in FLT3-ITD(+) lymphoid progenitor cells; lineage-specific STAT5 activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype in mice.
Methionine promoted casein synthesis, and this may be mediated by enhanced intracellular substrate availability and by activating JAK2-STAT5 and mTOR signaling pathways.
There was no association between the genotypes of GH and IGF-IS and fertility of Holstein cows raised in semiextensive or intensive regimes, while the STAT5 ABstEII polymorphism was associated with calving-first heat interval in Holstein cows raised in the intensive system.
Milk production traits were analyzed for each animal in the first, second, third, and fourth lactation. No genetic variability was found at STAT5A/AvaI locus. At STAT5A/MslI locus, the frequencies of T and C alleles were 0.875 and 0.125, respectively. Significant differences between genotypes were found
Results indicate that SNPs in STAT5A and JAK2 genes were associated with somatic cell count and score in milk and cytokines but none of the SNP was associated with milk production traits suggesting an important role in immunity.
The embryonic STAT5A gene is primarily activated by maternal gene products and the most abundant STAT5A expression occurred at the 2-cell stage blastocysts.
INVESTIGATION OF STAT5A, FSHR AND LHR GENE POLYMORPHISMS IN TURKISH INDIGENOUS CATTLE BREEDS
The Stat5a gene is associated with an increase in lactation of mammary gland epithelial cells.
STAT5A/AvaI polymorphism seems to be a promising indirect marker to improve milk production traits in cattle.
Associations between reproduction and milk traits, and polymorphisms at the STAT5A and FGF2 gene loci, were found with STAT5A polymorphism for age at first calving (suggestive effect; P =0.077) and lactation milk yield (significant effect; P<0.05).
Base sequence variation in STAT5A-noncoding region was studied.
The association of fertilization rate with STAT5A polymorphisms was evaluated in ocytes. Associations were found for 6 and 2 SNP. 5 SNP showed associations with both embryonic survival and fertilization rate compared with 1 SNP.
STAT5A affects embryonic survival in a manner influenced by developmental stage and allele parent of origin.
Although more studies are needed to better clarify the role of this SNP on production traits, STAT5A/AvaI polymorphism appears to be a promising indirect marker to improve milk production traits in cattle.
Mapped to chromosome 12 by radiation hybrid mapping.
This study indicates that CISH functions as a conserved in vivo target and regulator of STAT5 in the control of embryonic hematopoiesis.
study demonstrates that STAT5 in basophils is activated through both the IL-3 and the FcepsilonRI signaling pathway
Studies demonstrate a conserved role for SOCS1 in T cell development and suggest a novel T cell-independent function in embryonic myelopoiesis mediated, at least in part, via its effects on receptors using the Jak2-Stat5 pathway.
The stat5.1 gene lies next to the stat3 gene.
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. The mouse counterpart of this gene is found to induce the expression of BCL2L1/BCL-X(L), which suggests the antiapoptotic function of this gene in cells.
mammary gland factor STAT5A
, mammary gland factor
, signal transducer and activator of transcription 5
, STAT5A, Mammary Gland Factor
, signal transducer and activator of transcription 5A
, signal transducer and activator of transcription 5A-like
, signal transducer and activator of transcription 5B