gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

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, V1a, AGE
Papers on E3 ubiquitin ligase
Structure of a HOIP/E2~ubiquitin complex reveals RBR E3 ligase mechanism and regulation.
Riedl et al., Los Angeles, United States. In Nature, Feb 2016
The RBR family includes Parkin and HOIP, the central catalytic factor of the LUBAC (linear ubiquitin chain assembly complex).
Parkin promotes proteasomal degradation of p62: implication of selective vulnerability of neuronal cells in the pathogenesis of Parkinson's disease.
Chen et al., Tianjin, China. In Protein Cell, Feb 2016
UNASSIGNED: Mutations or inactivation of parkin, an E3 ubiquitin ligase, are associated with familial form or sporadic Parkinson's disease (PD), respectively, which manifested with the selective vulnerability of neuronal cells in substantia nigra (SN) and striatum (STR) regions.
Diabetic Cardiomyopathy: Role of the E3 Ubiquitin Ligase.
Cai et al., Jilin, China. In Am J Physiol Endocrinol Metab, Feb 2016
UNASSIGNED: Diabetic cardiomyopathy (DCM) is the leading cause of mortality in diabetes.
Advances in GBA-associated Parkinson's disease - pathology, presentation and therapies.
Grobler et al., Potchefstroom, South Africa. In Neurochem Int, Jan 2016
The Mendelian Parkinson's disease genes, Parkin and ATP13A2, intersect with glucocerebrosidase.
Parkin-mediated mitophagy directs perinatal cardiac metabolic maturation in mice.
Dorn et al., Saint Louis, United States. In Science, Jan 2016
Here, we found that PINK1-Mfn2-Parkin-mediated mitophagy directs this metabolic transformation in mouse hearts.
Role of mitophagy regulated by Parkin/DJ-1 in remote ischemic postconditioning-induced mitigation of focal cerebral ischemia-reperfusion.
Xue et al., Wuhan, China. In Eur Rev Med Pharmacol Sci, Dec 2015
OBJECTIVE: We evaluated the role of mitophagy controlled by Parkin/DJ-1 in remote ischemic post conditioning-induced mitigation of focal cerebral ischemia-reperfusion (I/R) injury in rats.
Targeting Pink1-Parkin-mediated mitophagy for treating liver injury.
Ding et al., Kansas City, United States. In Pharmacol Res, Dec 2015
Parkin is well-known to be required for mitophagy induction in in vitro models, and we previously showed that the Parkin-mediated mitophagy pathway likely plays a protective role against alcohol and acetaminophen-induced liver injuries.
In Vitro Comparison of the Activity Requirements and Substrate Specificity of Human and Triboleum castaneum PINK1 Orthologues.
Morais et al., Leuven, Belgium. In Plos One, Dec 2015
Nonetheless, both Tc and human PINK1 phosphorylate Parkin and Ubiquitin, two physiological substrates of PINK1.
Metformin Restores Parkin-Mediated Mitophagy, Suppressed by Cytosolic p53.
Lee et al., Seoul, South Korea. In Int J Mol Sci, Dec 2015
Here, we investigated the mechanism by which metformin induces mitophagy through restoration of the suppressed Parkin-mediated mitophagy.
Parkin-dependent mitophagy in the heart.
Dorn, Saint Louis, United States. In J Mol Cell Cardiol, Dec 2015
Here, the evidence supporting a role for the prototypical mitochondrial quality control pathway, PINK1-Parkin mediated mitophagy, in cardiac homeostasis and heart disease is reviewed.
Regulation of mitochondrial morphology and function by stearoylation of TFR1.
Teleman et al., Heidelberg, Germany. In Nature, Oct 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.
Mechanism of phospho-ubiquitin-induced PARKIN activation.
Komander et al., Cambridge, United Kingdom. In Nature, 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.
E3 Ubiquitin Ligase VHL Regulates Hypoxia-Inducible Factor-1α to Maintain Regulatory T Cell Stability and Suppressive Capacity.
Liu et al., Los Angeles, United States. In Immunity, Jul 2015
Here, we report that the E3 ubiquitin ligase VHL is essential for Treg cell function.
MIRO GTPases in Mitochondrial Transport, Homeostasis and Pathology.
Tang, Singapore, Singapore. In Cells, 2014
Recent findings have revealed a myriad of molecules that are associated with MIRO, particularly the kinesin adaptor Milton/TRAK, mitofusin, PINK1 and Parkin, as well as the endoplasmic reticulum-mitochondria encounter structure (ERMES) complex.
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
Biomarkers in Parkinson Disease: global gene expression analysis in peripheral blood from patients with and without mutations in PARK2 and PARK8.
Severino et al., São Paulo, Brazil. In Einstein (sao Paulo), 2010
METHODS: Global gene expression analysis by means of DNA microarrays was performed in peripheral blood of Parkinson disease patients with previously identified mutations in PARK2 or PARK8 genes, Parkinson disease patients without known mutations in these genes and normal controls.
share on facebooktweetadd +1mail to friends