期刊
MOLECULAR BIOLOGY OF THE CELL
卷 27, 期 7, 页码 1170-1180出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E16-01-0002
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资金
- Cornell University
- Medical Research Council
- National Institute for Health Research
- Wellcome Trust
- Wenner-Gren Foundations Fellowship
- MRC [MC_UU_12018/6] Funding Source: UKRI
- Medical Research Council [MC_UU_12018/6] Funding Source: researchfish
Membrane lipid dynamics must be precisely regulated for normal cellular function, and disruptions in lipid homeostasis are linked to the progression of several diseases. However, little is known about the sensory mechanisms for detecting membrane composition and how lipid metabolism is regulated in response to membrane stress. We find that phosphoinositide (PI) kinase signaling controls a conserved PDK-TORC2-Akt signaling cascade as part of a homeostasis network that allows the endoplasmic reticulum (ER) to modulate essential responses, including Ca2+-regulated lipid biogenesis, upon plasma membrane (PM) stress. Furthermore, loss of ER-PM junctions impairs this protective response, leading to PM integrity defects upon heat stress. Thus PI kinase-mediated ER-PM cross-talk comprises a regulatory system that ensures cellular integrity under membrane stress conditions.
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