Last update 01 Nov 2024

STAT5B

Last update 01 Nov 2024

Basic Info

Synonyms

Signal transducer and activator of transcription 5B, STAT5B

Introduction

Carries out a dual function: signal transduction and activation of transcription (PubMed:29844444). Mediates cellular responses to the cytokine KITLG/SCF and other growth factors. Binds to the GAS element and activates PRL-induced transcription. Positively regulates hematopoietic/erythroid differentiation.

Drugs associated with STAT5B

IST5-002

Target

STAT5A x STAT5B

Mechanism

STAT5A inhibitors [+1]

Active Org.

Thomas Jefferson University

Originator Org.

Thomas Jefferson University

Active Indication

Philadelphia chromosome positive chronic myelogenous leukemia [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AK-2292

Target

STAT5A x STAT5B

Mechanism

STAT5A inhibitors [+1]

Active Org.

University of Michigan

Originator Org.

University of Michigan

Active Indication

Acute Myeloid Leukemia

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with STAT5B

100 Translational Medicine associated with STAT5B

0 Patents (Medical) associated with STAT5B

1,295

Literatures (Medical) associated with STAT5B

01 Feb 2025·Blood Cells, Molecules, and Diseases

Growth hormone is involved in GATA1 gene expression via STAT5B in human erythroleukemia and monocytic cell lines

Article

Author: Moriyama, Kenji ; Matsushita, Midori ; Morita, Aoi ; Hano, Hiromi ; Mitsutani, Mana ; Tagami, Tetsuya ; Yokoyama, Mei

GATAs are a family of transcription factors consisting of six members. Particularly, GATA1 and GATA2 have been reported to promote the development of erythrocytes, megakaryocytes, eosinophils, and mast cells. However, little information is available on the extracellular ligands that promote GATA1 expression. We evaluated whether growth hormone (GH) is an extracellular stimulator that participates in the signal transduction of GATAs, focusing on GATA1 expression in hematopoietic cell lineages. We used a reporter assay, RT-PCR, real-time quantitative PCR, and western blotting to evaluate GH-induced expression of GATA1 and GATA2 in the human erythroleukemic cell line K562 and the non-erythroid cell line U937. GATA1 expression in these hematopoietic cell lines increased at the transcriptional and protein levels in the presence of GH, and was inhibited by a STAT5 specific inhibitor. Cells transfected with activated STAT5B showed increased expression of GATA1. We identified functional STAT5B consensus sequences as binding site-158 bp from the transcription starting site in the GATA1 promoter region. These results suggest that GH directly induces GATA1 expression via GHR/JAK/STAT5 and is related to hematopoietic cell proliferation.

31 Dec 2024·OncoImmunology

LFA-1 regulated by IL-2/STAT5 pathway boosts antitumor function of intratumoral CD8 ⁺ T cells for improving anti-PD-1 antibody therapy

Article

Author: Liu, Yaqing ; Shen, Chunyi ; Shan, Jiqi ; Liu, Fengsen ; Han, Dong ; Zhang, Yi ; Li, Congcong ; Jing, Wei ; Ping, Yu

Anti-PD-1 antibody therapy has achieved success in tumor treatment; however, the duration of its clinical benefits are typically short. The functional state of intratumoral CD8⁺ T cells substantially affects the efficacy of anti-PD-1 antibody therapy. Understanding how intratumoral CD8⁺ T cells change will contribute to the improvement in anti-PD-1 antibody therapy. In this study, we found that tumor growth was not arrested after the late administration of anti-PD-1 antibody and that the antitumor function of CD8⁺ T cells decreased with tumor progression. The results of the RNA sequencing of CD8⁺ T cells infiltrating the tumor site on days 7 and 14 showed that the cell adhesion molecule Lymphocyte Function-associated Antigen-1 (LFA-1) participates in regulating the antitumor function of CD8⁺ T cells and that decreased LFA-1 expression in intratumoral CD8⁺ T cells is associated with tumor progression. By analyzing the Gene Expression Omnibus (GEO) database and our results, we found that the antitumor function of intratumoral CD8⁺ T cells with high LFA-1 expression was stronger. The formation of immune synapses is impaired in Itgal-si CD8⁺ T cells, resulting in decreased anti-tumor function. LFA-1 expression in intratumoral CD8⁺ T cells is regulated by the IL-2/STAT5 pathway. The combination of IL-2 and anti-PD-1 antibody effectively enhanced LFA-1 expression and the antitumor function of intratumoral CD8⁺ T cells. The adoptive transfer of OT-1 T cells overexpressing LFA-1, STAT5A, or STAT5B resulted in higher antitumor function, deferred tumor growth, and prolonged survival. These findings indicate that LFA-1-mediated immune synapse acts as a regulator of the antitumor function of intratumoral CD8⁺ T cells, which can be applied to improve anti-PD-1 antibody therapy.

01 Dec 2024·The Journal of Nutritional Biochemistry

Chenodeoxycholic acid fortified diet drives ovarian steroidogenesis to improve embryo implantation through enhancing uterine receptivity via progesterone receptor signaling pathway in rats

Article

Author: Zhao, Xiaoyi ; Liu, Hui ; Zhu, Longlong ; Wang, Jing ; Zhang, Dongyang ; Chen, Meixia ; Chang, Zhuo ; Wang, Sixin

Infertility is a worldwide reproductive health problem influenced by the embryo implantation efficiency. We previously revealed that dietary chenodeoxycholic acid (CDCA) positively influence the early embryo implantation. But how CDCA regulate embryo implantation is largely unexplored. Herein, we investigated the mechanism behind CDCA's regulation on embryo implantation in rats. Results showed that CDCA promoted uterine receptivity, leading to increased number of implantation sites. Mechanistically, CDCA reshaped maternal amino acid metabolism and enhanced serum progesterone levels. CDCA enhanced ovarian progesterone synthesis by improving steroidogenesis-related protein (StAR and CYP11A1) expression via Takeda G-protein-coupled receptor 5. Elevated progesterone exaggerated uterine progesterone but weakened the estradiol signaling in the CDCA group, contributing to better uterine receptive for embryo implantation. Additionally, elevated transcription repressor Stat5b induced the down-regulation of progesterone-metabolizing enzyme 20-hydroxysteroid dehydrogenase 20α-HSD, complementally explained uterine progesterone signaling enhancement. Overall, our data revealed that CDCA drove ovarian steroidogenesis to improve embryo implantation through enhancing uterine receptivity via progesterone receptor pathway in rats. Therefore, CDCA diet may be a potential favorable nutritional strategy for infertility and pregnancy management.

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STAT5B

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