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we demonstrated that Imatinib mesylate (IM)impaired T cell survival through the inhibition of IL-7 (show IL7 Proteins) and STAT5-p but not TCR signaling which remained unaffected during IM therapy. Thus, off-target inhibitory effects of IM on IL-7 (show IL7 Proteins) 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 (show ABL1 Proteins), STAT5, JAK2 (show JAK2 Proteins), and STAT3 (show STAT3 Proteins) and downstream molecules including p-CrkL (show CRKL Proteins), Mcl-1 (show MCL1 Proteins), Bcl-XL (show BCL2L1 Proteins), and Bcl-2 (show BCL2 Proteins) proteins in K562 cells.
Two p53 (show TP53 Proteins) binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 (show TP53 Proteins) responsiveness in a luciferase reporter gene.
STAT3 (show STAT3 Proteins)/miR (show MLXIP Proteins)-211/STAT5A signaling plays a key role in mesenchymal stem cell migration.
Stat5 activation increased the DNA binding activity of NF-kappaB (show NFKB1 Proteins) though binding of p-Stat5 and p-RelA (show NFkBP65 Proteins) in nucleus.
these data suggest that ROCK2 (show ROCK2 Proteins) signaling plays a critical role in controlling the development of TFH cells induced by autoimmune conditions through reciprocal regulation of STAT3 (show STAT3 Proteins) 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 Proteins) 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 Proteins) 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.
Results suggest activation of H2AX (show H2AFX Proteins) 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 Proteins) 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 (show RPS6KB2 Proteins)) cells or CD150 (show SLAMF1 Proteins)+CD48 (show CD48 Proteins)- KLS (show RPS6KB2 Proteins) 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 Proteins) 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 Proteins) is dominant over STAT5A in CD4 (show CD4 Proteins)(+) '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 Proteins) resistance and lipotoxicity can be treated with ginsenoside Rg3, which acts though the STAT5-PPAR gamma (show PPARG Proteins) 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 Proteins) 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 Proteins) AND LHR (show LHCGR Proteins) 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 Proteins) 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 Proteins) functions as a conserved in vivo target and regulator of STAT5 (show STAT5B Proteins) in the control of embryonic hematopoiesis.
study demonstrates that STAT5 (show STAT5B Proteins) in basophils is activated through both the IL-3 (show IL-3 Proteins) and the FcepsilonRI (show FCER1G Proteins) signaling pathway
Studies demonstrate a conserved role for SOCS1 (show SOCS1 Proteins) 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 Proteins)-Stat5 (show STAT5B Proteins) pathway.
The stat5.1 (show STAT5B Proteins) gene lies next to the stat3 (show STAT3 Proteins) gene.
STAT5 (show STAT5B Proteins) 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