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Human STAT5A ELISA Kit for Cell ELISA - ABIN1981843
Park, Lee, Frank, Razani, Nguyen, Parlow, Russell, Hulit, Pestell, Lisanti: Caveolin-1-deficient mice show accelerated mammary gland development during pregnancy, premature lactation, and hyperactivation of the Jak-2/STAT5a signaling cascade. in Molecular biology of the cell 2002
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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 (show ABL1 ELISA Kits), STAT5, JAK2 (show JAK2 ELISA Kits), and STAT3 (show STAT3 ELISA Kits) and downstream molecules including p-CrkL (show CRKL ELISA Kits), Mcl-1 (show MCL1 ELISA Kits), Bcl-XL (show BCL2L1 ELISA Kits), and Bcl-2 (show BCL2 ELISA Kits) proteins in K562 cells.
Two p53 (show TP53 ELISA Kits) binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 (show TP53 ELISA Kits) responsiveness in a luciferase reporter gene.
STAT3 (show STAT3 ELISA Kits)/miR (show MLXIP ELISA Kits)-211/STAT5A signaling plays a key role in mesenchymal stem cell migration.
Stat5 activation increased the DNA binding activity of NF-kappaB (show NFKB1 ELISA Kits) though binding of p-Stat5 and p-RelA (show NFkBP65 ELISA Kits) in nucleus.
these data suggest that ROCK2 (show ROCK2 ELISA Kits) signaling plays a critical role in controlling the development of TFH cells induced by autoimmune conditions through reciprocal regulation of STAT3 (show STAT3 ELISA Kits) and STAT5 activation.
This is the first report of a survival disadvantage of EBV+ patients with CLL, and the first time that STAT5b (show STAT5B ELISA Kits) 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 (show STAT1 ELISA Kits) 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.
Results suggest activation of H2AX (show H2AFX ELISA Kits) 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 (show PDC ELISA Kits) 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 (show KIT ELISA Kits)+Lin-Sca-1 (show Ly6a ELISA Kits)+ (KLS (show RPS6KB2 ELISA Kits)) cells or CD150 (show SLAMF1 ELISA Kits)+CD48 (show CD48 ELISA Kits)- KLS (show RPS6KB2 ELISA Kits) 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 (show SOCS2 ELISA Kits) 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 (show STAT5B ELISA Kits) is dominant over STAT5A in CD4 (show CD4 ELISA Kits)(+) 'helper' T cells for both effector and regulatory (Treg) responses and, therefore, uniquely necessary for immunological tolerance.
Data indicate that obesity-induced insulin (show INS ELISA Kits) resistance and lipotoxicity can be treated with ginsenoside Rg3, which acts though the STAT5-PPAR gamma (show PPARG ELISA Kits) pathway in vivo and in vitro.
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 (show JAK2 ELISA Kits) 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 (show FSHR ELISA Kits) AND LHR (show LHCGR ELISA Kits) 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 (show FGF2 ELISA Kits) 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.
This study indicates that CISH (show CISH ELISA Kits) functions as a conserved in vivo target and regulator of STAT5 (show STAT5B ELISA Kits) in the control of embryonic hematopoiesis.
study demonstrates that STAT5 (show STAT5B ELISA Kits) in basophils is activated through both the IL-3 (show IL-3 ELISA Kits) and the FcepsilonRI (show FCER1G ELISA Kits) signaling pathway
Studies demonstrate a conserved role for SOCS1 (show SOCS1 ELISA Kits) 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 (show JAK2 ELISA Kits)-Stat5 (show STAT5B ELISA Kits) pathway.
The stat5.1 (show STAT5B ELISA Kits) gene lies next to the stat3 (show STAT3 ELISA Kits) gene.
STAT5 (show STAT5B ELISA Kits) functions in both primitive and definitive erythropoiesis, but by different mechanisms.
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
, signal transducer and activator of transcription 5B L homeolog