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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 (10) and many more products for this protein.
Showing 10 out of 176 products:
Human Monoclonal PARK2 Primary Antibody for IF, WB - ABIN393540
Kägi, Klein, Wood, Schneider, Pramstaller, Tadic, Quinn, van de Warrenburg, Bhatia: Nonmotor symptoms in Parkin gene-related parkinsonism. in Movement disorders : official journal of the Movement Disorder Society 2010
Show all 5 references for 393540
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
Show all 4 references for 407784
Human Polyclonal PARK2 Primary Antibody for FACS, IF - ABIN390365
West, Kapatos, OFarrell, Gonzalez-de-Chavez, Chiu, Farrer, Maidment: N-myc regulates parkin expression. in The Journal of biological chemistry 2004
Show all 2 references for 390365
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 references for 251684
Human Polyclonal PARK2 Primary Antibody for FACS, IF - ABIN390366
Wang, Denison, Lai, Philips, Montoya, Kock, Schüle, Klein, Shridhar, Roberts, Smith: Parkin gene alterations in hepatocellular carcinoma. in Genes, chromosomes & cancer 2004
Show all 2 references for 390366
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
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.
Human Mask homolog ANKHD1 (show ANKHD1 Antibodies) may serve as a potential therapeutic target for treating Parkinson disease caused by pink1 (show PINK1 Antibodies)/parkin mutations.
These results indicate that the in vivo rescue is due to restoring CI activity rather than promoting mitophagy Our findings support the emerging view that PINK1 (show PINK1 Antibodies) plays a role in regulating CI activity separate from its role with Parkin in mitophagy
MUL1 (show MUL1 Antibodies) acts in parallel to the PINK1 (show PINK1 Antibodies)/parkin pathway on a shared target mitofusin (show MFN2 Antibodies) to maintain mitochondrial integrity.
Parkin cooperates with PINK1 to promote hnRNP-F/Glo ubiquitination and nRCC mRNA translation.
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
Neurodegeneration in Parkinson's patients harboring homozygous loss-of-function mutations in the PARK2 gene may result from unbalanced levels of ROS (show ROS1 Antibodies), which are mostly produced in mitochondria and can irreparably damage macromolecules and trigger apoptosis.
These findings suggest that insufficient mitophagy-mediated PDGFR (show PDGFRB Antibodies)/PI3K (show PIK3CA Antibodies)/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
PKA-mediated phosphorylation of MIC60 negatively regulates mitochondrial clearance that is initiated by PINK1 (show PINK1 Antibodies) and Parkin.
This study found that Parkin-deficient animals do not accumulate senescent mitochondria in their motor axons or neuromuscular junctions.
Our study provided sufficient information and insight for investigation of PARK-2 and highlighted its role as a tumor suppressor gene in cervical cancer in North Indian population
The authors now report the crystal structure of a human Parkin-phosphoubiquitin complex, which shows that phosphoubiquitin binding induces movement in the 'in-between RING' (IBR) domain to reveal a cryptic ubiquitin-binding site.
Dopa-responsive dystonia phenotype may have heterogeneous genetic background and may be caused by point mutations or rearrangements in the GCH1 (show GCH1 Antibodies) gene as well as in the PARK2 gene.
study highlights the novel role of parkin in antiviral signaling
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