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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: Ubiquitin, PINK1, CAN, AGE, DJ-1
Papers on E3 ubiquitin ligase
Parkin and mitochondrial quality control: toward assembling the puzzle.
Winklhofer, Bochum, Germany. In Trends Cell Biol, Jun 2014
Parkin is an E3 ubiquitin ligase associated with autosomal-recessive Parkinsonism.
Lysine 27 ubiquitination of the mitochondrial transport protein miro is dependent on serine 65 of the Parkin ubiquitin ligase.
Kittler et al., London, United Kingdom. In J Biol Chem, Jun 2014
Moreover, Miro1 turnover on damaged mitochondria is altered in Parkinson 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 Ser65.
Muqit et al., Köln, Germany. In Biochem J, Jun 2014
We have previously reported that the Parkinson's disease-associated kinase PINK1 (PTEN-induced putative kinase 1) is activated by mitochondrial depolarization and stimulates the Parkin E3 ligase by phosphorylating Ser65 within its Ubl (ubiquitin-like) domain.
Mitochondrial quality control in neurodegenerative diseases.
Dupuis, Strasbourg, France. In Biochimie, May 2014
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.
Genetic mutations in early-onset Parkinson's disease Mexican patients: molecular testing implications.
López-López et al., Chiconcuac, Mexico. In Am J Med Genet B Neuropsychiatr Genet, Apr 2014
Mutations in PARK2, PINK1, and DJ-1 have been associated with autosomal recessive early-onset Parkinson's disease.
High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy.
Youle et al., 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.
Muqit et al., 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.
Das et al., 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.
Cox et al., 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.
A neo-substrate that amplifies catalytic activity of parkinson's-disease-related kinase PINK1.
Shokat et al., 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.
Weissman et al., 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.
Chen et al., 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.
Gehring et al., 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.
Dorn et al., 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.
Zekanowski et al., 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.
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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