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The precise function of PARK2 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. Additionally we are shipping PARK2 Kits (18) and PARK2 Proteins (11) and many more products for this protein.
Showing 10 out of 180 products:
Human Polyclonal PARK2 Primary Antibody for ICC, IF - ABIN407784
Eid, Ito, Otsuki: Triggering of Parkin Mitochondrial Translocation in Mitophagy: Implications for Liver Diseases. in Frontiers in pharmacology 2016
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Human Polyclonal PARK2 Primary Antibody for ELISA, WB - ABIN251684
La Cognata, Iemmolo, DAgata, Scuderi, Drago, Zappia, Cavallaro: Increasing the Coding Potential of Genomes Through Alternative Splicing: The Case of PARK2 Gene. in Current genomics 2014
Show all 2 Pubmed References
Human Polyclonal PARK2 Primary Antibody for IHC (p), IP - ABIN269703
Scuderi, La Cognata, Drago, Cavallaro, DAgata: Alternative splicing generates different parkin protein isoforms: evidences in human, rat, and mouse brain. in BioMed research international 2014
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Human Monoclonal PARK2 Primary Antibody for IF, WB - ABIN2476069
Ostby: [Fredrik Nightingale fellows]. in Journalen sykepleien 1990
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Human Polyclonal PARK2 Primary Antibody for IF (p), IHC (p) - ABIN735578
Li, Zhang, Wang, Liu, Yang, Liu, Lu: Neuroprotective effects of extract of Acanthopanax senticosus harms on SH-SY5Y cells overexpressing wild-type or A53T mutant ?-synuclein. in Phytomedicine : international journal of phytotherapy and phytopharmacology 2014
Human Monoclonal PARK2 Primary Antibody for IF, ELISA - ABIN562106
Brody, Taylor, Wilson, Delatycki, Lockhart: Regional and cellular localisation of Parkin co-regulated gene in developing and adult mouse brain. in Brain research 2008
Maintenance of tissue homeostasis upon reduction of Pink1 (show PINK1 Antibodies) or Parkin appears to result from reduction of age- and stress-induced intestinal stem cell proliferation, in part, through induction of ISC senescence.
activation of endoplasmic reticulum stress by defective mitochondria is neurotoxic in pink1 (show PINK1 Antibodies) and parkin flies and that the reduction of this signalling is neuroprotective, independently of defective mitochondria.
Pharmacological or genetic activation of heat shock protein 70 (Hsp70) protects against loss of parkin Function. Heat shock protein members may act as compensatory factors for parkin loss of function and that the exploitation of these factors may be of potential therapeutic value.
autophosphorylation of PINK1 (show PINK1 Antibodies) is essential for the mitochondrial translocation of Parkin and for subsequent phosphorylation and activation of Parkin.
Our data indicate that PINK1 (show PINK1 Antibodies) and Parkin play an important role in FUS (show FUS Antibodies)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (show FUS Antibodies) proteinopathy and PINK1 (show PINK1 Antibodies)/Parkin genes, providing new insights into the pathogenesis of FUS (show FUS Antibodies) proteinopathy.
Clu (show CLU Antibodies) is upstream of and binds to VCP (show vcp Antibodies) in vivo and promotes VCP (show vcp Antibodies)-dependent Marf (show MFN2 Antibodies) degradation in vitro Marf (show MFN2 Antibodies) accumulates in whole muscle lysates of clu (show CLU Antibodies)-deficient flies and is destabilized upon Clu (show CLU Antibodies) overexpression. Thus, Clu (show CLU Antibodies) is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP (show vcp Antibodies) for Marf (show MFN2 Antibodies) degradation to promote damaged mitochondrial clearance.
Buffy has a role enhancing the loss of parkin and suppressing the loss of Pink1 (show PINK1 Antibodies) phenotypes in Drosophila
Parkin-dependent mitophagy suppresses neural neurodegeneration by removing damaged mitochondria.
We demonstrate here that vps35 (show vps35 Antibodies) genetically interacts with parkin
Clu (show CLU Antibodies) directly modulates mitochondrial function, and that Clu's function contributes to the PINK1 (show PINK1 Antibodies)-Park pathway of mitochondrial quality control.
Melatonin, added together with MPTP (show PTPN2 Antibodies) or added once MPTP (show PTPN2 Antibodies) was removed, prevented and recovered, respectively, the parkinsonian phenotype once it was established, restoring gene expression and normal function of the parkin/PINK1 (show PINK1 Antibodies)/DJ-1 (show PARK7 Antibodies)/MUL1 loop and also the normal motor activity of the embryos.
These findings suggest that insufficient mitophagy-mediated PDGFR (show PDGFRB Antibodies)/PI3K/AKT (show AKT1 Antibodies) activation, which is mainly attributed to reduced PARK2 expression, is a potent underlying mechanism for myofibroblast differentiation and proliferation in fibroblastic foci formation during idiopathic pulmonary fibrosis pathogenesis
Mfn2 (show MFN2 Antibodies) downregulation or the exogenous expression of normal Parkin restored cytosolic Ca(2 (show CA2 Antibodies)+) transients in fibroblasts from patients with PARK2 mutations, a catalytically inactive Parkinson's disease (PD)-related Parkin variant had no effect. Parkin is directly involved in regulating ER-mitochondria contacts and provide new insight into the role of the loss of Parkin function in PD development
Our results provide a molecular explanation for the contribution of Drp1 (show CRMP1 Antibodies) to the pathogenesis of sporadic Parkinson's disease (PD). These findings indicate that the SNO-Parkin pathway may be a novel therapeutic target to treat PD
These results suggest a previously unidentified role of parkin in mediating endotoxin-induced endothelial proinflammatory signaling and indicate that it may play a critical role in acute inflammation.
These studies suggest that changes in intestinal lipid absorption may play a primary role in protection from nutritional stress in Park2 KO mice by preventing HFD-induced weight gain and highlight the need for tissue-specific models to address the role of PARK2 during metabolic stress.
Parkin negatively regulates the number and connectivity of mitochondria via a Drp1 (show CRMP1 Antibodies)-independent mechanism.
Parkin-overexpressing cells also showed reductions in apoptotic BAX (show BAX Antibodies) translocation to the mitochondria and cytochrome c (show CYCS Antibodies) release to the cytosol
Parkin protects against oxygen-glucose deprivation/reperfusion insult by promoting degradation of Drp1 (show CRMP1 Antibodies).
The identification of PINK1 (show PINK1 Antibodies) and Parkin as suppressors of an immune-response-eliciting pathway provoked by inflammation suggests new insights into Parkinson's disease pathology.
p62 (show GTF2H1 Antibodies) are subjected to parkin mediated proteasomal degradation
these results unveil a novel functional coupling between Parkin and the CaV2.2 (show CACNA1B Antibodies) channels.
These results demonstrate the feasibility of using UbFluor for quantitative studies of the biochemistry of RBR E3s and for high-throughput screening of small-molecule activators or inhibitors of PARKIN and other RBR E3 ligases.
data suggest that ROS (show ROS1 Antibodies) may act as a trigger for the induction of Parkin/PINK1 (show PINK1 Antibodies)-dependent mitophagy.
The proportions of some phospholipids and glycosphingolipids were altered in the lipid profiles of parkin-mutant skin fibroblasts obtained from Parkinson disease patients.
Adipogenic process can be dissected into 3 stages according to the participation of PARL (show PARL Antibodies)-PINK1 (show PINK1 Antibodies)-Parkin system. Findings reveal the sequential adipogenic events directed by PARL (show PARL Antibodies)-PINK1 (show PINK1 Antibodies)-Parkin system, add more evidence supporting the convergence of pathogenesis leading to neurodegenerative and metabolic disease
These results highlight the combined effects of Parkin and PGC-1alpha (show PPARGC1A Antibodies) in the maintenance of mitochondrial homeostasis in dopaminergic neurons. These two factors synergistically control the quality and function of mitochondria, which is important for the survival of neurons in Parkinson's disease.
Data suggest that inactivation of cytosolic parkin in dopaminergic neurons of the substantia nigra contributes to neurodegeneration in sporadic Parkinson disease. [REVIEW]
we identified a genome-wide significant association involving measures of midface height at 6q26 within an intron of PARK2
PARK2 inactivation connects energy and oxidative stress to Akt (show AKT1 Antibodies) activation via redox-mediated inactivation of PTEN (show PTEN Antibodies) by S-nitrosylation to support cell survival under conditions of energy deprivation.
These results suggest that degradation of endogenous APE1 (show APEX1 Antibodies) by Parkin occur when cells are stressed to activate Parkin, and imply a role of Parkin in maintaining the quality of APE1 (show APEX1 Antibodies), and loss of Parkin may contribute to elevated APE1 (show APEX1 Antibodies) levels in glioblastoma.
Single nucleotide polymorphism (SNP) analysis revealed seven SNPs in the porcine PARK2 gene, one missense and one silent mutation in exon 7 and five SNPs in intron 7
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.
, E3 ubiquitin-protein ligase parkin
, Parkinson disease (autosomal recessive, juvenile) 2, parkin
, parkin protein
, parkin variant SV5DEL
, parkinson juvenile disease protein 2