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This study indicates that CISH (show CISH Proteins) 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 (show Il3 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 pathway.
The stat5.1 gene lies next to the stat3 (show STAT3 Proteins) gene.
Results confirm that STAT5B is mutated in T-PLL and underscore the potential therapeutical relevance of epigenetic regulator.
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 and ICAM-1 (show ICAM1 Proteins) was significantly downregulated in PC3 (show PCSK1 Proteins) cells.
The two STAT5 (show STAT5A Proteins) isoforms, STAT5a (show STAT5A Proteins) and STAT5b.
support the concept that Jak2 (show JAK2 Proteins)-Stat5a (show STAT5A Proteins)/b signaling promotes metastatic progression of prostate cancer by inducing epithelial-to-mesenchymal transition and stem cell properties in prostate cancer cells
Interference of STAT (show STAT1 Proteins) 5b expression by siRNA targeting enhanced the chemo-sensitivity of gastric cancer cells to gefitinib by promoting mitochondrial pathway-mediated cell apoptosis.
Both Stat5a (show STAT5A Proteins)/b genetic knockdown and antiandrogen treatment induced proteasomal degradation of AR in prostate cancer cells.
Our study also assessed the regulation of signaling molecules implicated in the growth, progression, differentiation, and migration of cancer cells, such as Jak2 (show JAK2 Proteins), STAT5b, insulin (show INS Proteins)-like growth factor-1Rbeta, and their phosphorylation status
STAT3 (show STAT3 Proteins) and STAT5B mutations are associated with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK cells
These results indicated that STAT3 (show STAT3 Proteins) and STAT5b polymorphisms might be a candidate pharmacogenomic factor to assess susceptibility and prognosis in breast cancer patients.
Data indicate direct effects of sorafenib on the Janus kinase JAK1 (show JAK1 Proteins)-transcription factors STAT3 (show STAT3 Proteins)/5 signaling pathway in immune cells.
A study of the polymorphisms of STAT5b is presented, and the use of radiation hybrid mapping to localize the gene to chromosome 12 is presented.
SNPs in JAK2 (show JAK2 Proteins) and STAT5B are associated with mastitis susceptibility in Chinese Holstein cattle
This study suggests that growth hormone (show GH1 Proteins) inhibits the differentiation of bovine preadipocytes to adipocytes through STAT5b-dependent inhibition of C/EBPalpha (show CEBPA Proteins) and PPARgamma (show PPARG Proteins) expression.
These results suggested that the SNPs in CD4 (show CD4 Proteins) and STAT5b may be potential genetic markers for SCS (show TWIST1 Proteins) and milk/protein (show CSN2 Proteins) yields selecting and warrant further functional research.
STAT5B and MOF (show KAT8 Proteins) work as negative regulators in adipogenesis.
Strong selective advantage for leukemic transformation in the background of Stat5 (show STAT5A Proteins) deficient hematopoiesis was permissive for faster initiation of Myc (show MYC Proteins)-induced transformation to B (show TDO2 Proteins)-ALL.
liver STAT5b activation/masculinization occurred at puberty and suppression/feminization occurred during aging and in mutant mice with defects in growth hormone signaling.
Loss of STAT5b had no effect on either sex.
These data provide the first definitive evidence for a contribution of STAT5a (show STAT5A Proteins)/b to the sex bias in pulmonary hypertension in the hypoxic mouse and implicate reduced STAT5 (show STAT5A Proteins) in the pathogenesis of the human disease.
Data show that three hypotheses of dimer formation between STAT5 (show STAT5A Proteins) transcription factors STAT5A (show STAT5A Proteins) and STAT5B were used to explain the analytical results by a static mathematical model.
Increased expression of STAT5b + PDGFB (show PDGFB Proteins) led to increased expression of downstream STAT5b targets.
Expression of miR (show MLXIP Proteins)-21 is under prolactin (show PRL Proteins) control through the transcription factors STAT5A (show STAT5A Proteins)/B.
non-obese-diabetic genetic background is critical to the Stat5b-mediated lymphomagenesis through regulation of Stat5 (show STAT5A Proteins) hyperactivation
STAT5b but not STAT5a (show STAT5A Proteins) is the primary mediator of the action of prolactin (show PRL Proteins) in the hypothalamus.
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 5B
, signal transducer and activator of transcription 5B
, transcription factor STAT5B
, mammary gland factor STAT5B
, Signal transducer and activator of transcription 5a