GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 29 Mar 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)
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Top mentioned proteins:
Ubiquitin, PINK1, CAN, AGE, DJ-1
Papers on
E3 ubiquitin ligase
K27 ubiquitination of the mitochondrial transport protein Miro is dependent on serine 65 of the Parkin ubiquitin ligase.
New
London, United Kingdom. In J Biol Chem, 26 Apr 2014
Moreover Miro1 turnover on damaged mitochondria is altered in Parkinson's disease (PD) patient derived fibroblasts containing a pathogenic mutation in the PARK2 gene (encoding Parkin).
Parkin is activated by PINK1-dependent phosphorylation of ubiquitin at Serine65.
New
In Biochem J, 25 Apr 2014
UNLABELLED: We have previously reported that the Parkinson's disease associated PINK1 kinase is activated by mitochondrial depolarisation and stimulates the Parkin E3 ligase by phosphorylating Serine65 (Ser65) within its ubiquitin like (Ubl) domain.
Genetic mutations in early-onset Parkinson's disease Mexican patients: Molecular testing implications.
New
Chiconcuac, Mexico. In Am J Med Genet B Neuropsychiatr Genet, 23 Mar 2014
UNLABELLED: Mutations in PARK2, PINK1, and DJ-1 have been associated with autosomal recessive early-onset Parkinson's disease.
Parkin and mitochondrial quality control: toward assembling the puzzle.
Review
New
Bochum, Germany. In Trends Cell Biol, 02 Mar 2014
UNLABELLED: Parkin is an E3 ubiquitin ligase associated with autosomal-recessive Parkinsonism.
High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy.
New
Impact
Bethesda, United States. In Nature, Jan 2014
2) and parkin (PARK2, ref. 3) indicate that they may act in a quality control pathway preventing the accumulation of dysfunctional mitochondria.
Phosphorylation of Parkin at Serine65 is essential for activation: elaboration of a Miro1 substrate-based assay of Parkin E3 ligase activity.
New
Dundee, United Kingdom. In Open Biol, Dec 2013
Mutations in PINK1 and Parkin are associated with early-onset Parkinson's disease.
Antiaging Properties of a Grape-Derived Antioxidant Are Regulated by Mitochondrial Balance of Fusion and Fission Leading to Mitophagy Triggered by a Signaling Network of Sirt1-Sirt3-Foxo3-PINK1-PARKIN.
New
Farmington, United States. In Oxid Med Cell Longev, Dec 2013
PINK1 potentiates activation of PARKIN leading to the activation of mitochondrial fission and mitophagy.
The ubiquitin ligase parkin mediates resistance to intracellular pathogens.
New
Impact
San Francisco, United States. In Nature, Oct 2013
The parkin protein is a ubiquitin ligase with a well-established role in mitophagy, and mutations in the parkin gene (PARK2) lead to increased susceptibility to Parkinson's disease.
Mitochondrial quality control in neurodegenerative diseases.
Review
New
Strasbourg, France. In Biochimie, Sep 2013
UNLABELLED: Mutations causing genetic forms of Parkinson's disease or hereditary neuropathies have been recently shown to affect key molecular players involved in the recycling of defective mitochondria, most notably PARKIN, PINK1, Mitofusin 2 or dynein heavy chain.
A neo-substrate that amplifies catalytic activity of parkinson's-disease-related kinase PINK1.
New
Impact
San Francisco, United States. In Cell, Sep 2013
Moreover, we show that application of the KTP precursor kinetin to cells results in biologically significant increases in PINK1 activity, manifest as higher levels of Parkin recruitment to depolarized mitochondria, reduced mitochondrial motility in axons, and lower levels of apoptosis.
Compact Parkin only: insights into the structure of an autoinhibited ubiquitin ligase.
Review
New
Frederick, United States. In Embo J, Aug 2013
Mutations in Parkin represent ~50% of disease-causing defects in autosomal recessive-juvenile onset Parkinson's disease (AR-JP).
Molecular signaling toward mitophagy and its physiological significance.
Review
New
Zhanjiang, China. In Exp Cell Res, Aug 2013
Considerable advancements have been made to elucidate the molecular mechanism behind mitophagy, particularly Parkin-mediated mitophagy.
Structure of parkin reveals mechanisms for ubiquitin ligase activation.
New
Impact
Montréal, Canada. In Science, Jul 2013
Mutations in the PARK2 (parkin) gene are responsible for an autosomal recessive form of Parkinson's disease.
PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria.
New
Impact
Saint Louis, United States. In Science, May 2013
Senescent and damaged mitochondria undergo selective mitophagic elimination through mechanisms requiring two Parkinson's disease factors, the mitochondrial kinase PINK1 (PTEN-induced putative kinase protein 1; PTEN is phosphatase and tensin homolog) and the cytosolic ubiquitin ligase Parkin.
Integrated pathways of parkin control over mitochondrial maintenance - relevance to Parkinson's disease pathogenesis.
Review
Warsaw, Poland. In Acta Neurobiol Exp (wars), 2012
Here, we focus on the deficiency of PARK2 and its product parkin, which is relevant to both familial and sporadic PD pathogenesis.
Meta-analysis of the influence of Parkin p.Asp394Asn variant on the susceptibility of Parkinson's disease.
GeneRIF
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
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
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
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
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
