کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2204687 1100810 2012 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Bidirectional crosstalk between endoplasmic reticulum stress and mTOR signaling
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Bidirectional crosstalk between endoplasmic reticulum stress and mTOR signaling
چکیده انگلیسی

Many cellular processes including apoptosis, autophagy, translation, energy metabolism, and inflammation are controlled by the mammalian target of rapamycin (mTOR) kinase and the endoplasmic reticulum (ER) stress pathway, also known as the unfolded protein response (UPR). Although both of these signaling nodes have attracted wide attention in fundamental cell biology and drug discovery, crosstalk between the two pathways has emerged only very recently. mTOR complex 1 (mTORC1) operates both upstream and downstream of ER stress signals, which can either enhance or antagonize the anabolic output of mTORC1. Upon prolonged ER stress, mTORC1 contributes to apoptotic signaling by suppressing the survival kinase Akt through feedback inhibition. Likewise, chronic ER stress obstructs activation of Akt by mTOR complex 2. This review surveys our knowledge of mTOR–ER stress intersections and highlights potential therapeutic implications.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 22, Issue 5, May 2012, Pages 274–282
نویسندگان
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