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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 11 Dec 2014.

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
Upregulation of parkin in endophilin mutant mice.
De Camilli et al., Genova, Italy. In J Neurosci, 03 Jan 2015
Endophilin, a key factor in the endocytosis of synaptic vesicles, was shown to bind to, and be ubiquitinated by, the PD-linked E3 ubiquitin ligase Parkin.
Glutamate excitotoxicity in neurons triggers mitochondrial and endoplasmic reticulum accumulation of Parkin, and, in the presence of N-acetyl cysteine, mitophagy.
Berman et al., Pittsburgh, United States. In Neurobiol Dis, 02 Jan 2015
Parkin, the product of gene PARK2 whose mutation causes familial PD, has been linked to mitochondrial quality control via its role in regulating mitochondrial dynamics, including mitochondrial degradation via mitophagy.
Phosphorylation of Mitochondrial Polyubiquitin by PINK1 Promotes Parkin Mitochondrial Tethering.
Imai et al., Tokyo, Japan. In Plos Genet, 31 Dec 2014
The kinase PINK1 and the E3 ubiquitin (Ub) ligase Parkin participate in mitochondrial quality control.
Inflammation is genetically implicated in Parkinson's disease.
Halliday et al., Sydney, Australia. In Neuroscience, 22 Nov 2014
Relatively rare missense mutations in genes such as LRRK2, Parkin, SNCA and PINK1 are causative for familial PD whereas more common variation in genes, including LRRK2, SNCA and GBA, comprise risk factors for sporadic PD.
Choline dehydrogenase interacts with SQSTM1/p62 to recruit LC3 and stimulate mitophagy.
Jung et al., Seoul, South Korea. In Autophagy, Sep 2014
Knockdown of CHDH expression impairs CCCP-induced mitophagy and PARK2/parkin-mediated clearance of mitochondria in mammalian cells, including HeLa cells and SN4741 dopaminergic neuronal cells.
A new pathway for mitochondrial quality control: mitochondrial-derived vesicles.
McBride et al., Montréal, Canada. In Embo J, Sep 2014
The Parkinson's disease-associated proteins Vps35, Parkin, and PINK1 are involved in the biogenesis of a subset of these MDVs, linking this novel trafficking pathway to human disease.
The diabetes susceptibility gene Clec16a regulates mitophagy.
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.
The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy.
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.
Ubiquitin is phosphorylated by PINK1 to activate parkin.
Matsuda et al., Tokyo, Japan. In Nature, Jul 2014
PINK1 (PTEN induced putative kinase 1) and PARKIN (also known as PARK2) have been identified as the causal genes responsible for hereditary recessive early-onset Parkinsonism.
PARK2 orchestrates cyclins to avoid cancer.
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.
[The role of parkin in Parkinson's disease].
Pencz et al., Budapest, Hungary. In Neuropsychopharmacol Hung, Jun 2014
Parkin (Parkinson juvenile disease protein 2) is a ~52 kDa (426 amino acid) enzyme protein, encoded by PARK2 gene and located on the 6q chromosome.
Parkin and PINK1: much more than mitophagy.
Dawson et al., Baltimore, United States. In Trends Neurosci, Jun 2014
In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets.
Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins.
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.
Behavioral phenotyping of parkin-deficient mice: looking for early preclinical features of Parkinson's disease.
Prediger et al., Florianópolis, Brazil. In Plos One, Dec 2013
Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient mice do not display spontaneous degeneration of the nigrostriatal pathway or enhanced vulnerability to dopaminergic neurotoxins such as 6-OHDA and MPTP.
Genetics of Parkinson's disease - a clinical perspective.
Kim et al., Pusan, South Korea. In J Mov Disord, 2012
Discovering genes following Medelian inheritance, such as autosomal dominant-synuclein and leucine-rich repeat kinase 2 gene, or autosomal recessive Parkin, P-TEN-induced putative kinase 1 gene and Daisuke-Junko 1 gene, has provided great insights into the pathogenesis of Parkinson's disease (PD).
Meta-analysis of the influence of Parkin p.Asp394Asn variant on the susceptibility of Parkinson's disease.
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.
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.
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.
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).
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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