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Somatic STAT5B N642H gain-of-function mutation in early onset nonclonal eosinophilia, urticaria, dermatitis, and diarrhea in two young patients.
High incidence of activating STAT5B mutations in CD4 (zeige CD4 Proteine)-positive T-cell large granular lymphocyte leukemia.
STAT5 signaling drives antigen restimulation-induced T cell death in effector memory T cells
Data show that BACH2 (zeige BACH2 Proteine) and STAT5B are activated by viral insertions, generating chimeric mRNAs specifically enriched in T regulatory cells favoring their persistence.
The findings, specifically frequent mutations of STAT5B, PIK3CD, and the histone methyltransferase SETD2, may help guide translational efforts to target hepatosplenic T-cell lymphoma
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 (zeige STAT5A Proteine) 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 (zeige STAT1 Proteine) agents.
STAT5 (zeige STAT5A Proteine) signaling axis drives abnormal cell proliferation in autosomal dominant polycystic kidney disease.
p65 (zeige GORASP1 Proteine) activation triggered by TCR signaling could promote SNRPA (zeige SNRPA Proteine) transcription and 3' UTR shortening of STAT5B. Thus we propose that the alternative polyadenylation switching of STAT5B induced by TCR activation is mediated by SNRPA (zeige SNRPA Proteine).
this study shows that musculin (zeige MSC Proteine) inhibits human T-helper 17 cell response to interleukin 2 (zeige IL2 Proteine) by controlling STAT5B activity
Molecular interactions of EphA4 (zeige EPHA4 Proteine), growth hormone receptor (zeige GHR Proteine), Jak2 (zeige JAK2 Proteine), and STAT5B have been described.
STAT5B is a crucial regulator of RICD in memory T cells in mice
Our work is the first to report that an active form of Stat5b restored DCs tolerogenic functions that re-educated Tregs to re-establish and to sustain long-term protective immune response against diabetes in NOD mice.
Instead, we find that STAT5B is dominant over STAT5A (zeige STAT5A Proteine) in CD4 (zeige CD4 Proteine)(+) 'helper' T cells for both effector and regulatory (Treg) responses and, therefore, uniquely necessary for immunological tolerance.
These studies establish the importance of STAT5 (zeige STAT5A Proteine) in macrophages during ductal morphogenesis in the mammary gland and demonstrate that altering STAT5 (zeige STAT5A Proteine) function in macrophages can affect the development of tissue-specific disease.
Data indicate that 89% of signal transducer and activator of transcription 5 (zeige STAT5A Proteine) (Stat5b)-CA mice in which the T2/Onc transposon had been mobilized died of progenitor B-cell acute lymphoblastic leukemia (B-ALL) by 3 months of age.
STAT5B and MOF (zeige KAT8 Proteine) work as negative regulators in adipogenesis.
Strong selective advantage for leukemic transformation in the background of Stat5 (zeige STAT5A Proteine) deficient hematopoiesis was permissive for faster initiation of Myc (zeige MYC Proteine)-induced transformation to B (zeige TDO2 Proteine)-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.
SNPs in JAK2 (zeige JAK2 Proteine) and STAT5B are associated with mastitis susceptibility in Chinese Holstein cattle
This study suggests that growth hormone (zeige GH1 Proteine) inhibits the differentiation of bovine preadipocytes to adipocytes through STAT5b-dependent inhibition of C/EBPalpha (zeige CEBPA Proteine) and PPARgamma (zeige PPARG Proteine) expression.
These results suggested that the SNPs in CD4 (zeige CD4 Proteine) and STAT5b may be potential genetic markers for SCS (zeige TWIST1 Proteine) and milk/protein (zeige CSN2 Proteine) yields selecting and warrant further functional research.
This study indicates that CISH (zeige CISH Proteine) 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 (zeige IL-3 Proteine) and the FcepsilonRI (zeige FCER1G Proteine) signaling pathway
Studies demonstrate a conserved role for SOCS1 (zeige SOCS1 Proteine) 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 (zeige JAK2 Proteine)-Stat5 pathway.
The stat5.1 gene lies next to the stat3 (zeige STAT3 Proteine) gene.
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.
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.
transcription factor STAT5B
, Signal transducer and activator of transcription 5a
, mammary gland factor STAT5B
, signal transducer and activator of transcription 5B
, signal transducer and activator of transcription 5A
, Signal transducer and activator of transcription 5B