A Novel ER Stress-Independent Function of the UPR in Angiogenesis

被引：44

作者：

Urra, Hery ^{[1
,2
]}

Hetz, Claudio ^{[1
,2
,3
,4
]}

机构：

[1] Univ Chile, Fac Med, Biomed Neurosci Inst, Santiago 7, Chile

[2] Univ Chile, Inst Biomed Sci, Program Cellular & Mol Biol, Ctr Mol Studies Cell, Santiago, Chile

[3] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

[4] Neuroun Biomed Fdn, Santiago, Chile

来源：

MOLECULAR CELL | 2014年 / 54卷 / 04期

关键词：

UNFOLDED PROTEIN RESPONSE;

D O I：

10.1016/j.molcel.2014.05.013

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Tumors rely on the unfolded protein response (UPR) and angiogenesis to survive the metabolic stress of hypoxia. Karali et al. (2014) revealed that VEGF signaling engages UPR sensors in an unconventional manner that is independent of endoplasmic reticulum (ER) stress, mediated by mTOR signaling to promote endothelial cell survival and angiogenesis.

引用

收藏

页码：542 / 544

页数：3

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