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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
Interactions between genetic variants and dietary lipid composition: effects on circulating LDL cholesterol in children.
Raitakari et al., Turku, Finland. In Am J Clin Nutr, 31 Dec 2014
RESULTS: In the STRIP cohort, a variant within the PARK2 locus, rs9364628, showed moderate interaction with dietary fat quality and a consistent direction of effect in both scans on serum LDL-cholesterol concentration in children aged 5 and 7 y (P < 0.0084 and P < 0.0057, respectively).
Cyclin-dependent Kinase 1 (CDK1)-dependent Inhibition of the E3 Ubiquitin Ligase, CRL4CDT2, Ensures Robust Transition from S Phase to Mitosis.
Cook et al., Hopkins, United States. In J Biol Chem, 19 Dec 2014
UNLABELLED: Replication-coupled destruction of a cohort of cell cycle proteins ensures efficient and precise genome duplication.
The Complex I Subunit NDUFA10 Selectively Rescues Drosophila pink1 Mutants through a Mechanism Independent of Mitophagy.
Whitworth et al., Sheffield, United Kingdom. In Plos Genet, 30 Nov 2014
Substantial evidence indicates that PINK1 acts with another PD gene, parkin, to regulate mitochondrial morphology and mitophagy.
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.
[Alpha-synuclein in Parkinson's disease].
Dorszewska et al., In Przegl Lek, Dec 2013
It is believed, that causes of PD are both environmental and genetic factors, associated mainly with mutations in the SNCA and PRKN genes, which may lead to changes in the structure of proteins such as alpha-synuclein (ASN) and Parkin.
Acute focal brain damage alters mitochondrial dynamics and autophagy in axotomized neurons.
D'Amelio et al., Roma, Italy. In Cell Death Dis, Dec 2013
We provided evidence that lesion of a cerebellar hemisphere causes mitochondria depolarization in axotomized precerebellar neurons associated with PTEN-induced putative kinase 1 accumulation and Parkin translocation to mitochondria, block of mitochondrial fusion by Mfn1 degradation, increase of calcineurin activity and dynamin-related protein 1 translocation to mitochondria, and consequent mitochondrial fission.
High-Content Functional Genomic Screening to Identify Novel Regulators of the PINK1-Parkin Pathway.
Screaton et al., Ottawa, Canada. In Methods Enzymol, Dec 2013
PINK1/PARK6 and Parkin/PARK2 are amongst the most commonly mutated genes associated with recessive forms of familial Parkinson's disease.
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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