title: RNA metabolism in the pathogenesis of Parkinson׳s disease.
abstract: Neurodegenerative diseases such as Parkinson׳s disease are progressive disorders of the nervous system that affect the function and maintenance of specific neuronal populations. While most disease cases are sporadic with no known cause, a small percentage of disease cases are caused by inherited genetic mutations. The identification of genes associated with the familial forms of the diseases and subsequent studies of proteins encoded by the disease genes in cellular or animal models have offered much-needed insights into the molecular and cellular mechanisms underlying disease pathogenesis. Recent studies of the familial Parkinson׳s disease genes have emphasized the importance of RNA metabolism, particularly mRNA translation, in the disease process. It is anticipated that continued studies on the role of RNA metabolism in Parkinson׳s disease will offer unifying mechanisms for understanding the cause of neuronal dysfunction and degeneration and facilitate the development of novel and rational strategies for treating this debilitating disease.
authors.affiliation: Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, United States. Electronic address: bingwei@stanford.edu.
authors.forename: Bingwei
authors.initials: B
authors.lastname: Lu
authors.affiliation: Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, United States.
authors.forename: Stephan
authors.initials: S
authors.lastname: Gehrke
authors.affiliation: Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, United States.
authors.forename: Zhihao
authors.initials: Z
authors.lastname: Wu
mesh_terms: D000818:Animals; D039603:Eukaryotic Initiation Factor-4G / Q000235:genetics; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D000071158:Leucine-Rich Repeat Serine-Threonine Protein Kinase-2; D009154:Mutation; D015513:Oncogene Proteins / Q000235:genetics; D010300:Parkinson Disease / Q000235:genetics* / Q000378:metabolism*; D014176:Protein Biosynthesis; D000071617:Protein Deglycase DJ-1; D011494:Protein Kinases / Q000235:genetics; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D012313:RNA / Q000235:genetics* / Q000378:metabolism*; D015398:Signal Transduction; D044767:Ubiquitin-Protein Ligases / Q000235:genetics; D051844:alpha-Synuclein / Q000235:genetics; D000099202:PTEN-Induced Putative Kinase
chemical_list: D039603:Eukaryotic Initiation Factor-4G; D047908:Intracellular Signaling Peptides and Proteins; D000071158:Leucine-Rich Repeat Serine-Threonine Protein Kinase-2; D015513:Oncogene Proteins; D000071617:Protein Deglycase DJ-1; D011494:Protein Kinases; D017346:Protein Serine-Threonine Kinases; D012313:RNA; D044767:Ubiquitin-Protein Ligases; D051844:alpha-Synuclein; D000099202:PTEN-Induced Putative Kinase; C113920:EIF4G1 protein, human; C111567:parkin protein; C495280:LRRK2 protein, human; C105131:PARK7 protein, human
keywords: MicroRNAs; Mitochondria; Oxidative stress; Parkinson׳s disease; Translation initiation; mRNA metabolism; mTOR signaling