期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1802, 期 1, 页码 11-19出版社
ELSEVIER
DOI: 10.1016/j.bbadis.2009.07.007
关键词
Mitochondrial import; Outer membrane translocase; Amyloid precursor protein; Alpha synuclein; Mitochondrial dysfunction; Alzheimer's disease; Parkinson' disease
资金
- Alzheimer's Association [IIRG-08-89896]
- NIH [R01 AG 021920]
- NATIONAL INSTITUTE ON AGING [R01AG021920] Funding Source: NIH RePORTER
Mitochondrial dysfunction is an important intracellular lesion associated with a wide variety of diseases including neurodegenerative disorders. In addition to aging, oxidative stress and mitochondrial DNA mutations, recent studies have implicated a role for the mitochondrial accumulation of proteins such as plasma membrane associated amyloid precursor protein (APP) and cytosolic alpha synuclein in the pathogenesis of mitochondrial dysfunction in Alzheimer's disease (AD) and Parkinson's disease (PD), respectively. Both of these proteins contain cryptic mitochondrial targeting signals, which drive their transport across mitochondria. In general, mitochondrial entry of nuclear coded proteins is assisted by import receptors situated in both outer and inner mitochondrial membranes. A growing number of evidence suggests that APP and alpha synclein interact with import receptors to gain entry into mitochondrial compartment. Additionally, carboxy terminal cleaved product of APP, similar to 4 kDa Abeta, is also transported into mitochondria with the help of mitochondrial outer membrane import receptors. This review focuses on the mitochondrial targeting and accumulation of these two structurally different proteins and the mode of mechanism by which they affect the physiological functions of mitochondria. (C) 2009 Elsevier B.V. All rights reserved.
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