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JAK/STAT信号通路中的蛋白酪氨酸磷酸酶

Protein tyrosine phosphatases in the JAK/STAT pathway.

作者信息

Xu Dan, Qu Cheng-Kui

机构信息

Department of Medicine, Division of Hematology/Oncology, Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio 44106, USA.

出版信息

Front Biosci. 2008 May 1;13:4925-32. doi: 10.2741/3051.

DOI:10.2741/3051
PMID:18508557
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2599796/
Abstract

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is crucial in controlling cellular activities in response to extracellular cytokines. Dysfunctions of the JAK/STAT pathway result in various hematopoietic and immune disorders. The central events in regulating this pathway are tyrosine phosphorylation and dephosphorylation of the signaling components, which are carried out by protein tyrosine kinases and protein tyrosine phosphatases (PTP), respectively. Here, we review recent advances in the regulatory roles of PTPs, in particular, SHP2 phosphatase, in the JAK/STAT signaling pathway.

摘要

Janus激酶(JAK)/信号转导及转录激活因子(STAT)通路在控制细胞对细胞外细胞因子的反应活动中至关重要。JAK/STAT通路功能失调会导致多种造血和免疫紊乱。调节该通路的核心事件是信号成分的酪氨酸磷酸化和去磷酸化,分别由蛋白酪氨酸激酶和蛋白酪氨酸磷酸酶(PTP)执行。在此,我们综述了PTP,特别是SHP2磷酸酶,在JAK/STAT信号通路中的调节作用的最新进展。

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本文引用的文献

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JAK-STAT signaling: from interferons to cytokines.JAK-STAT信号传导:从干扰素到细胞因子
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TC-PTP-deficient bone marrow stromal cells fail to support normal B lymphopoiesis due to abnormal secretion of interferon-{gamma}.由于干扰素-γ分泌异常,缺乏酪氨酸磷酸酶非受体型C的骨髓基质细胞无法支持正常的B淋巴细胞生成。
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