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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 06 Mar 2015.

Parkinson protein 2, E3 ubiquitin protein ligase

E3 ubiquitin ligase, Parkin, PARK2
The precise function of this gene is unknown; however, the encoded protein is a component of a multiprotein E3 ubiquitin ligase complex that mediates the targeting of substrate proteins for proteasomal degradation. Mutations in this gene are known to cause Parkinson disease and autosomal recessive juvenile Parkinson disease. Alternative splicing of this gene produces multiple transcript variants encoding distinct isoforms. Additional splice variants of this gene have been described but currently lack transcript support. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PINK1, Ubiquitin, CAN, DJ-1, AGE
Papers on E3 ubiquitin ligase
USP30 deubiquitylates mitochondrial Parkin substrates and restricts apoptotic cell death.
New
Urbé et al., Bilbao, Spain. In Embo Rep, 04 Apr 2015
The unique mitochondrial deubiquitylase, USP30, opposes Parkin-dependent ubiquitylation of TOM20, and its depletion enhances depolarization-induced cell death in Parkin-overexpressing cells.
Doxorubicin induces apoptosis in Jurkat cells by mitochondria-dependent and mitochondria-independent mechanisms under normoxic and hypoxic conditions.
New
Jimenez-Del-Rio et al., Medellín, Colombia. In Anticancer Drugs, 02 Apr 2015
In addition, dxr (10 μmol/l) induced activation and/or nuclei translocation of NF-κB (6.6, 1.6-fold increase), p53 (4.3, 3.1 f), c-Jun (9.5, 5.0 f), apoptosis-inducing factor (AIF) (1.9, 3.9 f), caspase-3 (3.7, 1.9 f), overexpression of Parkin (2.1, 1.2 f)/PINK-1 (2.1 f) proteins, and reduced DJ-1 levels by half compared with untreated cells under normoxia, according to immunofluorescence and in-cell western analysis, respectively.
N-acetylcysteine prevents rotenone-induced Parkinson's disease in rat: an investigation into the interaction of Parkin and Drp1 proteins.
New
Hassanzadeh et al., Sanandaj, Iran. In Brain Res Bull, 27 Mar 2015
Western blot analysis was also done for parkin and Drp1 (dynamin related protein-1) proteins quantification in SN and ST.
Molecular mechanisms underlying PINK1 and Parkin catalyzed ubiquitylation of substrates on damaged mitochondria.
Review
New
Matsuda et al., Tokyo, Japan. In Biochim Biophys Acta, 17 Mar 2015
UNASSIGNED: PINK1 and Parkin are gene products that cause genetic recessive Parkinsonism.
PINK1/Parkin-mediated mitophagy in mammalian cells.
Review
New
Okamoto et al., Suita, Japan. In Curr Opin Cell Biol, 16 Mar 2015
In mammalian cells, the Ser/Thr kinase PINK1 and the E3 ubiquitin ligase Parkin act cooperatively in sensing mitochondrial functional state and marking damaged mitochondria for disposal via the autophagy pathway.
Autophagy machinery in the context of mammalian mitophagy.
Review
New
Mizushima et al., Tokyo, Japan. In Biochim Biophys Acta, 26 Feb 2015
PINK1-Parkin-dependent mitophagy has been extensively studied in the mammalian system.
The Roles of PINK1, Parkin, and Mitochondrial Fidelity in Parkinson's Disease.
Review
New
Youle et al., Bethesda, United States. In Neuron, 21 Feb 2015
PINK1 accumulates on the outer membrane of damaged mitochondria, activates Parkin's E3 ubiquitin ligase activity, and recruits Parkin to the dysfunctional mitochondrion.
PINK1 and Parkin control localized translation of respiratory chain component mRNAs on mitochondria outer membrane.
New
Impact
Lu et al., Stanford, United States. In Cell Metab, 06 Feb 2015
Here we show that Parkinson's disease (PD)-associated genes PINK1 and Parkin direct localized translation of certain nuclear-encoded RCC (nRCC) mRNAs.
Anthracycline-containing chemotherapy causes long-term impairment of mitochondrial respiration and increased reactive oxygen species release in skeletal muscle.
New
Jagoe et al., Montréal, Canada. In Sci Rep, Dec 2014
Mitochondrial DNA content and protein levels of key mitochondrial membrane proteins and markers of mitochondrial biogenesis were unchanged, but protein levels of Parkin were reduced.
Mitochondrial homeostasis molecules: regulation by a trio of recessive Parkinson's disease genes.
Review
New
Son et al., Seoul, South Korea. In Exp Neurobiol, Dec 2014
In this mini-review, we provide an overview of the mitochondrial quality control mechanisms, emphasizing regulatory molecules in mitophagy and biogenesis that specifically interact with the protein products of three major recessive familial PD genes, PINK1, Parkin and DJ-1.
Correction: Behavioral Phenotyping of Parkin-Deficient Mice: Looking for Early Preclinical Features of Parkinson's Disease.
New
The PLOS ONE Staff, In Plos One, Dec 2014
UNASSIGNED: [This corrects the article DOI: 10.1371/journal.pone.0114216.].
The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy.
New
Impact
Sheng et al., San Francisco, United States. In Nature, Jul 2014
Here we report that USP30, a deubiquitinase localized to mitochondria, antagonizes mitophagy driven by the ubiquitin ligase parkin (also known as PARK2) and protein kinase PINK1, which are encoded by two genes associated with Parkinson's disease.
The diabetes susceptibility gene Clec16a regulates mitophagy.
New
Impact
Stoffers et al., Philadelphia, United States. In Cell, Jul 2014
Here we report that Clec16a is a membrane-associated endosomal protein that interacts with E3 ubiquitin ligase Nrdp1.
Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins.
New
Impact
Chan et al., New York City, United States. In Nat Genet, Jun 2014
The PARK2 E3 ubiquitin ligase coordinately controls the stability of both cyclin D and cyclin E. Analysis of approximately 5,000 tumor genomes shows that PARK2 is a very frequently deleted gene in human cancer and uncovers a striking pattern of mutual exclusivity between PARK2 deletion and amplification of CCND1, CCNE1 or CDK4-implicating these genes in a common pathway.
PARK2 orchestrates cyclins to avoid cancer.
New
Impact
Hodny et al., Praha, Czech Republic. In Nat Genet, Jun 2014
A new study identifies the PARK2 E3 ubiquitin ligase as an important coordinator of G1/S-phase cyclin turnover and explains how mutations targeting this key cell cycle regulatory node contribute to a range of cancers.
Meta-analysis of the influence of Parkin p.Asp394Asn variant on the susceptibility of Parkinson's disease.
GeneRIF
Sun et al., Beijing, China. In Neurosci Lett, 2012
This study does not support an association between the Parkin p.Asp394Asn variant and Parkinson disease risk.
PARK2 gene mutations in early onset Parkinson's disease patients of South India.
GeneRIF
Ramesh et al., Chennai, India. In Neurosci Lett, 2012
mutations in PARK2 gene may be a common cause of Parkinson's disease among South Indian early onset patients.
High frequency of Parkin exon rearrangements in Mexican-mestizo patients with early-onset Parkinson's disease.
GeneRIF
López López et al., Chiconcuac, Mexico. In Mov Disord, 2012
Patients with parkin exons 9 and 12 rearrangements showed a later age at onset than did cases with other regions affected, suggesting a mutational hot spot in the etiology of Mexican-mestizo patients with early-onset Parkinson's disease
Analysis of neural subtypes reveals selective mitochondrial dysfunction in dopaminergic neurons from parkin mutants.
GeneRIF
Pallanck et al., Seattle, United States. In Proc Natl Acad Sci U S A, 2012
study validates key tenets of the model that PINK1 and Parkin promote the fragmentation and turnover of depolarized mitochondria in dopaminergic neurons
Lewy body pathology and typical Parkinson disease in a patient with a heterozygous (R275W) mutation in the Parkin gene (PARK2).
GeneRIF
Giaccone et al., Milano, Italy. In Acta Neuropathol, 2012
report a patient with a heterozygous Parkin mutation (R275W, on exon 7), clinical features of typical Parkinson's disease and a neuropathological picture of diffuse Lewy body disease
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