期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1833, 期 1, 页码 176-183出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2012.08.004
关键词
OPA1; Mitochondria; Membrane dynamics; Apoptosis; mtDNA; Dominant optic atrophy
资金
- CNRS
- Universite Paul Sabatier
- Retina-France
- AFM
- AMMI
- Ligue Contre le Cancer
- UNADEV
- ARC
- Region Midi-Pyrenees
- CIHR [MOP-82718]
- FRSQ
The studies addressing the molecular mechanisms governing mitochondrial fusion and fission have brought to light a small group of dynamin-like GTPases (Guanosine-Triphosphate hydrolase) as central regulators of mitochondrial morphology and cristae remodeling, apoptosis, calcium signaling, and metabolism. One of them is the mammalian OPA1 (Optic atrophy 1) protein, which resides inside the mitochondrion anchored to the inner membrane and, in a cleaved form, is associated to oligomeric complexes, in the intermembrane space of the organelle. Here, we review the studies that have made OPA1 emerge as the best understood regulator of mitochondrial inner membrane fusion and cristae remodeling. Further, we re-examine the findings behind the recent claim that OPA1 mediates adrenergic control of lipolysis by functioning as a cytosolic A-kinase anchoring protein (AKAP), on the hemimembrane that envelops the lipid droplet. This article is part of a Special Issue entitled: Mitochondrial dynamics and physiology. (c) 2012 Elsevier B.V. All rights reserved.
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