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STAT5 activation by EGF (show EGF Proteins) constitutes an important cascade for the regulation of cell proliferation and invasion in trophoblast cells.
Decreased expression of STAT5 was associated with metastases in Colon Carcinoma.
MSM decreased the ability of STAT5b (show STAT5B Proteins) to bind the promoter of the HER2 (show ERBB2 Proteins) gene.
PTP1B (show PTPN1 Proteins) directly regulates STAT5 phosphorylation and its activation via the cAMP/PKA pathway downstream of the 5-HT7 (show HTR7 Proteins) receptor is involved in the suppression of beta-casein (show CSN2 Proteins) expression in MCF-12A cells
Foxp3 (show FOXP3 Proteins) has a rapid turn over in Treg partly controlled at the transcriptional level by the JAK (show JAK3 Proteins)/STAT (show STAT1 Proteins) pathway
Results confirm that STAT5B (show STAT5B Proteins) is mutated in T-PLL and underscore the potential therapeutical relevance of epigenetic regulator.
prolactin (show PRL Proteins) activation of Stat5 results in the formation of a complex between phospho-Stat5 and BRCA1. Formation of this complex does not interfere with nuclear translocation or binding of BRCA1 to the p21 (show CDKN1A Proteins) promoter
ABL (show ABL1 Proteins)-N administration induced apoptosis of PC3 (show PCSK1 Proteins) cells in a dose-dependent manner, along with the enhanced activity of caspases and increased Bax (show BAX Proteins)/Bcl-2 (show BCL2 Proteins) ratio. Expression of KLF5 (show KLF5 Proteins), Stat5b (show STAT5B Proteins) and ICAM-1 (show ICAM1 Proteins) was significantly downregulated in PC3 (show PCSK1 Proteins) cells.
The innate immune regulator STAT-5 is shown to regulate transcription of the ATR binding factor TopBP1, and this is critical for the induction of the ATR pathway in human papillomavirus-infected keratinocytes.
The two STAT5 isoforms, STAT5a and STAT5b (show STAT5B Proteins).
constitutive STAT5 binding to c-Myc (show MYC Proteins) super-enhancer might contribute to BRD2 (show BRD2 Proteins) maintenance and thus allow sustained expression of c-Myc (show MYC Proteins) in Ba/F3 cells transformed by STAT5-1*6.
transduction of developing Th9 cells with a constitutively active STAT5 eliminates the ability of IL-6 (show IL6 Proteins) to reduce IL-9 (show IL9 Proteins) production.
Strong selective advantage for leukemic transformation in the background of Stat5 deficient hematopoiesis was permissive for faster initiation of Myc (show MYC Proteins)-induced transformation to B (show TDO2 Proteins)-ALL.
Thrombopoietin (show THPO Proteins)-mediated phosphorylation of STAT5 triggers its genome-wide relocation to STAT (show STAT1 Proteins) consensus sites, resulting in loss of a uSTAT5 program that restrains megakaryocytic differentiation and activation of STAT5-driven gene expression.
Transcriptome analysis identified a class of mammary-restricted genes that was particularly dependent on high STAT5 levels as a result of the intergenic enhancer
domain-mapping results showed that both the substrate-interacting and the phosphatase domains of DUSP4 (show DUSP9 Proteins) were required for its optimal interaction with STAT5, while the coiled-coil domain of STAT5 appeared to hinder this interaction
STAT5 activation by FLT3 (show FLT3 Proteins)-ITD protects cells treated with the PI3K/Akt (show AKT1 Proteins) pathway inhibitors from apoptosis by maintaining Mcl-1 (show MCL1 Proteins) expression through the mTORC1/4EBP1 (show EIF4EBP1 Proteins)/eIF4E (show EIF4E Proteins) pathway.
Collectively, the findings show that human beta-cells fail to proliferate in response to PRL (show PRL Proteins) for multiple reasons, one of which is a paucity of functional PRL (show PRL Proteins) receptors, and that murine Stat5 overexpression is able to bypass these impediments.
STAT5 signaling is increased in the liver in GH-transgenic mice during the growth period, with a balance between positive and negative effectors resulting in accelerated but controlled growth.
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.
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.
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.
signal transducer and activator of transcription 5A
, signal transducer and activator of transcription 5A-like
, mammary gland factor STAT5A
, mammary gland factor
, signal transducer and activator of transcription 5
, STAT5A, Mammary Gland Factor
, transcription factor STAT5B