Browse our anti-STAT5B (STAT5B) Antibodies

Human Signal Transducer and Activator of Transcription 5B (STAT5B) interaction partners

1. STAT5B promoted cell proliferation and drug resistance in human Mantle cell lymphoma cells by activating the Akt signaling pathway.

2. Herein, we emphasize the aggressive nature of STAT5B(N642H) in driving T-cell neoplasia upon hematopoietic expression in transgenic mice, revealing evidence of multiple T-cell subset organ infiltration. Notably, we demonstrate STAT5B(N642H)-driven transformation of gammadelta T-cells in in vivo syngeneic transplant models, comparable to STAT5B(N642H) patient gammadelta T-cell entities.

3. Recurrent activating STAT5B N642H mutation is associated with myeloid neoplasms with eosinophilia.

4. data suggest that JAK and Aurora kinase inhibitors should be further explored as potential therapeutics for lymphoma and leukemia patients with the STAT5BN642H mutation who respond poorly to conventional chemotherapy.

5. Increased expression of proteins STAT5B, GRB2, and OXSR1 was related to a higher probability of metastasis. Multivariate analysis demonstrated that tumor grade and STAT5B were independent prognostic factors.

6. findings indicated that cAMP-PKA up-regulated STAT5B, followed by increase in syncytin2 expression through GCM1 and OVOL1, resulting in cell fusion and hCG production, while cAMP-PKA-up-regulated NR4A3 could decrease syncytin2 expression.

7. CSF3R T618I, ASXL1 G942 fs and STAT5B N642H trimutation co-contribute to a rare chronic neutrophilic leukaemia manifested by rapidly progressive leucocytosis, severe infections, persistent fever and deep venous thrombosis.

8. STAT5B germline mutation variants exert dominant-negative effects through distinct pathomechanisms, manifesting in milder clinical growth hormone insensitivity syndrome with general sparing of the immune system.

9. Study investigated whether RGS4 could participate in signalling pathways to regulate neurotropic events. These observations suggest that RGS4 is implicated in opioid dependent neuronal differentiation and neurite outgrowth via a "non-canonical" signaling pathway regulating STAT5B-directed responses.

10. Our finding supports that STAT3 was the potential treated target for breast cancer therapy, whereas STAT5A/5B/6 were potential prognostic markers for better survival of BC, providing more accurate prognosis.

11. Somatic STAT5B N642H gain-of-function mutation in early onset nonclonal eosinophilia, urticaria, dermatitis, and diarrhea in two young patients.

12. High incidence of activating STAT5B mutations in CD4-positive T-cell large granular lymphocyte leukemia.

13. STAT5 signaling drives antigen restimulation-induced T cell death in effector memory T cells

14. Data show that BACH2 and STAT5B are activated by viral insertions, generating chimeric mRNAs specifically enriched in T regulatory cells favoring their persistence.

15. The findings, specifically frequent mutations of STAT5B, PIK3CD, and the histone methyltransferase SETD2, may help guide translational efforts to target hepatosplenic T-cell lymphoma

16. 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 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 agents.

17. STAT5 signaling axis drives abnormal cell proliferation in autosomal dominant polycystic kidney disease.

18. p65 activation triggered by TCR signaling could promote SNRPA 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.

19. this study shows that musculin inhibits human T-helper 17 cell response to interleukin 2 by controlling STAT5B activity

20. Molecular interactions of EphA4, growth hormone receptor, Jak2, and STAT5B have been described.

Mouse (Murine) Signal Transducer and Activator of Transcription 5B (STAT5B) interaction partners

1. data suggest that JAK and Aurora kinase inhibitors should be further explored as potential therapeutics for lymphoma and leukemia patients with the STAT5BN642H mutation who respond poorly to conventional chemotherapy.

2. study enables us to conclude that beta-cell stress is aggravated by the incapability of STAT5B to induce Nos2 resulting in HO accumulation and the ensuing oxidative stress enhances beta-cell damage.

3. Study used a gene expression biomarker that can accurately predict the activation status of the oxidant-induced transcription factor Nrf2 in a microarray database and uncovered a strong linkage between increased Nrf2 activity and feminization of the male liver mediated by suppression of STAT5b. Examination of female versus male comparisons showed that Nrf2 is subtly but reproducibly activated to higher levels in females.

4. NK cell numbers are decreased in Stat5a-Stat5b tetramer-deficient double knockin mice, but the mechanism was not investigated. Here we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-associated genes

5. Study investigated whether RGS4 could participate in signalling pathways to regulate neurotropic events. These observations suggest that RGS4 is implicated in opioid dependent neuronal differentiation and neurite outgrowth via a "non-canonical" signaling pathway regulating STAT5B-directed responses.

6. STAT5B is a crucial regulator of RICD in memory T cells in mice

7. 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.

8. Instead, we find that STAT5B is dominant over STAT5A in CD4(+) 'helper' T cells for both effector and regulatory (Treg) responses and, therefore, uniquely necessary for immunological tolerance.

9. STAT5 signaling axis drives abnormal cell proliferation in autosomal dominant polycystic kidney disease.

10. These studies establish the importance of STAT5 in macrophages during ductal morphogenesis in the mammary gland and demonstrate that altering STAT5 function in macrophages can affect the development of tissue-specific disease.

11. Data indicate that 89% of signal transducer and activator of transcription 5 (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.

12. STAT5B and MOF work as negative regulators in adipogenesis.

13. Strong selective advantage for leukemic transformation in the background of Stat5 deficient hematopoiesis was permissive for faster initiation of Myc-induced transformation to B-ALL.

14. liver STAT5b activation/masculinization occurred at puberty and suppression/feminization occurred during aging and in mutant mice with defects in growth hormone signaling.

15. Loss of STAT5b had no effect on either sex.

16. These data provide the first definitive evidence for a contribution of STAT5a/b to the sex bias in pulmonary hypertension in the hypoxic mouse and implicate reduced STAT5 in the pathogenesis of the human disease.

17. Data show that three hypotheses of dimer formation between STAT5 transcription factors STAT5A and STAT5B were used to explain the analytical results by a static mathematical model.

18. Increased expression of STAT5b + PDGFB led to increased expression of downstream STAT5b targets.

19. Expression of miR-21 is under prolactin control through the transcription factors STAT5A/B.

20. non-obese-diabetic genetic background is critical to the Stat5b-mediated lymphomagenesis through regulation of Stat5 hyperactivation

Cow (Bovine) Signal Transducer and Activator of Transcription 5B (STAT5B) interaction partners

1. SNPs in JAK2 and STAT5B are associated with mastitis susceptibility in Chinese Holstein cattle

2. This study suggests that growth hormone inhibits the differentiation of bovine preadipocytes to adipocytes through STAT5b-dependent inhibition of C/EBPalpha and PPARgamma expression.

3. These results suggested that the SNPs in CD4 and STAT5b may be potential genetic markers for SCS and milk/protein yields selecting and warrant further functional research.

Pig (Porcine) Signal Transducer and Activator of Transcription 5B (STAT5B) interaction partners

1. 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.