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内质网应激与驻留 PTP1B 的原位功能。

Endoplasmic reticulum stress and the on site function of resident PTP1B.

机构信息

Institute of Cellular Biology and Pathology N. Simionescu of the Romanian Academy 8, B.P. Hasdeu Street, Bucharest 050568, Romania.

出版信息

Biochem Biophys Res Commun. 2012 Jun 15;422(4):535-8. doi: 10.1016/j.bbrc.2012.05.048. Epub 2012 May 15.

DOI:10.1016/j.bbrc.2012.05.048
PMID:22609202
Abstract

Growing evidence links the stress at the endoplasmic reticulum (ER) to pathologies such as diabetes mellitus, obesity, liver, heart, renal and neurodegenerative diseases, endothelial dysfunction, atherosclerosis, and cancer. Therefore, identification of molecular pathways beyond ER stress and their appropriate modulation might alleviate the stress, and direct toward novel tools to fight this disturbance. An interesting resident of the ER membrane is protein tyrosine phosphatase 1B (PTP1B), an enzyme that negatively regulates insulin and leptin signaling, contributing to insulin and leptin resistance. Recently, new functions of PTP1B have been established linked to ER stress response. This review evaluates the novel data on ER stressors, discusses the mechanisms beyond PTP1B function in the ER stress response, and emphasizes the potential therapeutic exploitation of PTP1B to relieve ER stress.

摘要

越来越多的证据将内质网(ER)的压力与糖尿病、肥胖症、肝脏、心脏、肾脏和神经退行性疾病、血管内皮功能障碍、动脉粥样硬化和癌症等病理学联系起来。因此,识别 ER 应激之外的分子途径及其适当的调节可能会减轻这种压力,并为对抗这种干扰提供新的工具。内质网膜上的一个有趣的驻留蛋白是蛋白酪氨酸磷酸酶 1B(PTP1B),它是一种负调节胰岛素和瘦素信号的酶,导致胰岛素和瘦素抵抗。最近,PTP1B 的新功能已被确定与 ER 应激反应有关。本文评价了 ER 应激原的新数据,讨论了 PTP1B 在 ER 应激反应中的功能之外的机制,并强调了利用 PTP1B 缓解 ER 应激的潜在治疗潜力。

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