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非磷酸化 STAT3 的研究进展:综述

Advances in research on unphosphorylated STAT3: A review.

作者信息

Zhang Lei, Guo Wei, Lu Na, Tian Yuqing, Yang Jinghua, Wang Liang

机构信息

Research Center of Traditional Chinese Medicine and Clinical Pharmacy, Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao University, Jinan, China.

出版信息

Medicine (Baltimore). 2025 Jul 25;104(30):e43476. doi: 10.1097/MD.0000000000043476.

DOI:10.1097/MD.0000000000043476
PMID:40725945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12303475/
Abstract

Signal transducer and activator of transcription 3 (STAT3), a member of the STAT family, is a pivotal player in multiple cellular processes including proliferation, migration, differentiation, angiogenesis, programmed cell death, inflammatory response, and immune activation. As a transcription factor, the regulation of STAT3 activity is incredibly complicated as it is implicated signaling pathways in many distinct types of cells and under a diverse array of conditions. The activation of STAT3 commonly depends on the phosphorylation of specific residues in response to numerous growth factors and cytokines. With the discovery of STAT3 mediating gene expression in the absence of tyrosine/serine phosphorylation, a growing number of investigations related to unphosphorylated signal transducer and activator of transcription 3 (U-STAT3) demonstrated that U-STAT3 possess distinct features in regulation of gene expression. Herein, we summarize the current research progress in the roles of U-STAT3 in transcription and try to provide a basis for better understanding the complicated STAT3 activity regulation and its diverse functions.

摘要

信号转导与转录激活因子3(STAT3)是STAT家族的一员,在多种细胞过程中起着关键作用,包括增殖、迁移、分化、血管生成、程序性细胞死亡、炎症反应和免疫激活。作为一种转录因子,STAT3活性的调节极其复杂,因为它涉及许多不同类型细胞在多种条件下的信号通路。STAT3的激活通常依赖于特定残基的磷酸化,以响应多种生长因子和细胞因子。随着在酪氨酸/丝氨酸未磷酸化情况下STAT3介导基因表达的发现,越来越多与未磷酸化信号转导与转录激活因子3(U-STAT3)相关的研究表明,U-STAT3在基因表达调控中具有独特的特征。在此,我们总结了U-STAT3在转录作用方面的当前研究进展,并试图为更好地理解复杂的STAT3活性调节及其多样功能提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93fb/12303475/b5ad712aac21/medi-104-e43476-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93fb/12303475/b5ad712aac21/medi-104-e43476-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/93fb/12303475/b5ad712aac21/medi-104-e43476-g001.jpg

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本文引用的文献

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Structure of the SNAPc-bound RNA polymerase III preinitiation complex.与SNAPc结合的RNA聚合酶III起始前复合物的结构。
Cell Res. 2023 Jul;33(7):565-568. doi: 10.1038/s41422-023-00819-x. Epub 2023 May 10.
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STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis.STAT3 通过调控 miR-106a-5p/TP73 轴促进 RNA 聚合酶 III 指导的转录。
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Polygalaxanthone III, an Active Ingredient in , Repaired -Stimulated Skin Injury via STAT3 Phosphorylated Activation.
三叶胶酮 III,一种来自 的活性成分,通过 STAT3 磷酸化激活修复刺激的皮肤损伤。
Molecules. 2022 Nov 3;27(21):7520. doi: 10.3390/molecules27217520.
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The Roles of Post-Translational Modifications in STAT3 Biological Activities and Functions.翻译后修饰在STAT3生物学活性和功能中的作用
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The pleiotropic role of transcription factor STAT3 in oncogenesis and its targeting through natural products for cancer prevention and therapy.转录因子STAT3在肿瘤发生中的多效性作用及其通过天然产物进行靶向以预防和治疗癌症。
Med Res Rev. 2020 Dec 1. doi: 10.1002/med.21761.
6
Manipulation of JAK/STAT Signalling by High-Risk HPVs: Potential Therapeutic Targets for HPV-Associated Malignancies.高危型 HPV 对 JAK/STAT 信号通路的调控:HPV 相关恶性肿瘤的潜在治疗靶点。
Viruses. 2020 Sep 3;12(9):977. doi: 10.3390/v12090977.
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Genome-wide blood DNA methylation analysis in patients with delayed cerebral ischemia after subarachnoid hemorrhage.蛛网膜下腔出血后迟发性脑缺血患者全基因组血液 DNA 甲基化分析。
Sci Rep. 2020 Jul 10;10(1):11419. doi: 10.1038/s41598-020-68325-3.
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Downregulation of microRNA‑106a‑5p alleviates ox‑LDL‑mediated endothelial cell injury by targeting STAT3.下调 microRNA-106a-5p 通过靶向 STAT3 缓解 ox-LDL 介导的内皮细胞损伤。
Mol Med Rep. 2020 Aug;22(2):783-791. doi: 10.3892/mmr.2020.11147. Epub 2020 May 14.
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Targeting STAT3 signaling pathway in cancer by agents derived from Mother Nature.靶向源自大自然的药物抑制肿瘤 STAT3 信号通路。
Semin Cancer Biol. 2022 May;80:157-182. doi: 10.1016/j.semcancer.2020.03.016. Epub 2020 Apr 20.
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Cell Commun Signal. 2020 Feb 28;18(1):33. doi: 10.1186/s12964-020-0527-z.