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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 28 Aug 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, AGE, V1a
Papers on E3 ubiquitin ligase
Mechanism of phospho-ubiquitin-induced PARKIN activation.
New
Impact
Komander et al., Cambridge, United Kingdom. In Nature, 20 Sep 2015
The E3 ubiquitin ligase PARKIN (encoded by PARK2) and the protein kinase PINK1 (encoded by PARK6) are mutated in autosomal-recessive juvenile Parkinsonism (AR-JP) and work together in the disposal of damaged mitochondria by mitophagy.
How phosphoubiquitin activates Parkin E3 activity.
New
Hunter et al., Los Angeles, United States. In Cell Res, 11 Sep 2015
UNASSIGNED: A recent report, solving the structure of a Parkin-phosphoubiquitin complex, greatly advances the understanding of the Parkin activation mechanism.
Site-specific Interaction Mapping of Phosphorylated Ubiquitin to Uncover Parkin Activation.
New
Matsuda et al., Tokyo, Japan. In J Biol Chem, 10 Sep 2015
A cytosolic E3 ubiquitin ligase Parkin, a gene product mutated in familial Parkinsonism, is essential for this pathway.
E3 Ubiquitin Ligase NEDD4 Promotes Influenza Virus Infection by Decreasing Levels of the Antiviral Protein IFITM3.
New
Yount et al., Columbus, United States. In Plos Pathog, 31 Aug 2015
Here, we demonstrate that the E3 ubiquitin ligase NEDD4 ubiquitinates IFITM3 in cells and in vitro.
Regulation of mitochondrial morphology and function by stearoylation of TFR1.
New
Impact
Teleman et al., Heidelberg, Germany. In Nature, 27 Aug 2015
Intriguingly, dietary C18:0 supplementation can counteract the mitochondrial dysfunction caused by genetic defects such as loss of the Parkinson's disease genes Pink or Parkin in Drosophila.
E3 Ubiquitin Ligase VHL Regulates Hypoxia-Inducible Factor-1α to Maintain Regulatory T Cell Stability and Suppressive Capacity.
New
Impact
Liu et al., Los Angeles, United States. In Immunity, 16 Jul 2015
Here, we report that the E3 ubiquitin ligase VHL is essential for Treg cell function.
AMPK activation of muscle autophagy prevents fasting-induced hypoglycemia and myopathy during aging.
New
Impact
Steinberg et al., Hamilton, Canada. In Cell Metab, 02 Jul 2015
Consistent with impaired autophagy, aged AMPK-MKO mice possess a significant myopathy characterized by reduced muscle function, mitochondrial disease, and accumulation of the autophagy/mitophagy proteins p62 and Parkin.
Mitochondrial Dysfunction in Parkinson's Disease.
Review
New
Paek et al., Seoul, South Korea. In Exp Neurobiol, Jun 2015
For the first time, we established human telomerase reverse transcriptase (hTERT)-immortalized wild type, idiopathic and Parkin deficient mesenchymal stromal cells (MSCs) isolated from the adipose tissues of PD patients, which could be used as a good cellular model to evaluate mitochondrial dysfunction for the better understanding of PD pathology and for the development of early diagnostic markers and effective therapy targets of PD.
How mitochondrial dynamism orchestrates mitophagy.
Review
New
Dorn et al., Beersheba, Israel. In Circ Res, Jun 2015
Here, we review accumulating evidence supporting important roles for mitochondrial fission and fusion in cardiac mitochondrial quality control, focusing on the PTEN-induced putative kinase 1-Parkin mitophagy pathway.
Quantifying ubiquitin signaling.
Review
New
Harper et al., Boston, United States. In Mol Cell, Jun 2015
Here, we review how quantitative proteomic tools and enrichment strategies are being used to quantify UB-dependent signaling systems, and to integrate UB signaling with regulatory phosphorylation events, illustrated with the PINK1/PARKIN pathway.
The three 'P's of mitophagy: PARKIN, PINK1, and post-translational modifications.
Review
New
Fon et al., Montréal, Canada. In Genes Dev, Jun 2015
Two Parkinson's disease (PD)-associated proteins, the mitochondrial kinase PINK1 and the E3-ubiquitin (Ub) ligase PARKIN, are central to mitochondrial quality control.
Phosphatase and tensin homolog-induced putative kinase 1 and Parkin in diabetic heart: Role of mitophagy.
Review
New
Long et al., Xi'an, China. In J Diabetes Investig, May 2015
Phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and Parkin, initially identified to be associated with the pathogenesis of a familiar form of Parkinson's disease, have recently been recognized to play a critical role in mediating cardiomyocytes' adaption to stresses.
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, 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.
Parkinson's Disease in Saudi Patients: A Genetic Study.
New
Al Tassan et al., Riyadh, Saudi Arabia. In Plos One, Dec 2014
Here we investigated the genetic causes of PD in Saudis by recruiting 98 PD-cases (sporadic and familial) and screening them for potential pathogenic mutations in PD-established genes; SNCA, PARKIN, PINK1, PARK7/DJ1, LRRK2 and other PD-associated genes using direct sequencing.
Protective Effect of Sevoflurane Postconditioning against Cardiac Ischemia/Reperfusion Injury via Ameliorating Mitochondrial Impairment, Oxidative Stress and Rescuing Autophagic Clearance.
New
Xu et al., Nanchang, China. In Plos One, Dec 2014
Meanwhile, SPC significantly suppressed the decline of Opa1 and increases of Drp1 and Parkin induced by I/R injury (P < 0.05 vs. I/R group).
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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