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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 (19) 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 IHC (p), IP - ABIN269703
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 ELISA, WB - ABIN251684
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 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
Human Monoclonal PARK2 Primary Antibody for IF, WB - ABIN2476069
Ostby: [Fredrik Nightingale fellows]. in Journalen sykepleien 1990
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This study found learning and memory abnormalities in Parkin mutant genotypes in Drosophila.
parkin mutants have a longer lifespan when fed the 1:16 P:C compared to those fed the 1:2 P:C diet. Parkin mutants fed the 1:16 P:C diet have delayed climbing deficit, increased resistance to starvation. Mutant flies fed the 1:16 P:C diet also have improved mitochondrial functions as evidenced by increased respiratory control ratio
Drosophila CHIP protects against mitochondrial dysfunction by acting downstream of Pink1 (show PINK1 Antibodies) in parallel with Parkin
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 was found to interact with p53 (show TP53 Antibodies); however, this was abolished in Parkin KO mice model, which prevented p53 (show TP53 Antibodies) degradation reducing inflammatory arthritis.
These findings unveil an important role of Parkin in protecting genome stability through positively regulating translesion DNA synthesis (TLS (show FUS Antibodies)) upon UV damage, providing a novel mechanistic link between Parkin deficiency and predisposition to skin cancers in PD patients.
Thus, the present study indicated that parkin knockout inhibits neural stem cell differentiation by JNK (show MAPK8 Antibodies)-dependent proteasomal degradation of p21 (show CDKN1A Antibodies).
Parkin hyper-activation by pUb(S57 (show CD81 Antibodies)) demonstrates the first PINK1 (show PINK1 Antibodies)-independent route to active parkin, revealing the roles of multiple ubiquitin phosphorylation sites in governing parkin stimulation and catalytic activity.
the results of this study suggest that mutations on specific genes (PARK2 and LRRK2) compromising basal ganglia functioning may be subtly related to language-processing mechanisms.
MicroRNA-181a has a role in suppressing parkin-mediated mitophagy and sensitizing neuroblastoma (show ARHGEF16 Antibodies) cells to mitochondrial uncoupler-induced apoptosis
Findings suggest that PARK2 might have a tumor suppressor role in the development of chronic obstructive pulmonary disease (COPD (show ARCN1 Antibodies)) and lung cancer.
Here we review the evidence supporting PINK1 (show PINK1 Antibodies)/Parkin mitophagy in vivo and its causative role in neurodegeneration, and outline outstanding questions for future investigations.
Although PARK2 may be a pathological factor for neurodevelopmental disorders , likely not all variants are pathogenic, and a conclusive assessment of PARK2 variant pathogenicity requires an accurate analysis of their location within the coding region and encoded functional domains.
VPS35 (show vps35 Antibodies) regulates parkin substrate AIMP2 (show AIMP2 Antibodies) toxicity by facilitating lysosomal clearance of AIMP2 (show AIMP2 Antibodies).
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.
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
crossed Parkin knockouts to the Twinkle-TG mouse in which mtDNA deletions are increased specifically in substantia nigra to determine the effect of increased deletion mutagenesis in the absence of mitochondrial quality control
These findings reveal parkin-mediated cytoprotective mechanisms against misfolded SOD1 (show SOD1 Antibodies) toxicity.
Park2 deficiency exacerbates ethanol-induced dopaminergic neuron damage through p38 (show CRK Antibodies) kinase dependent inhibition of autophagy and mitochondrial function.
PARK2-dependent acidic postconditioning -induced mitophagy renders the brain resistant to ischemic injury.
Our results indicate that strict maternal transmission of mitochondria relies on mitophagy and uncover a collaboration between MUL1 (show MUL1 Antibodies) and PARKIN in this process.
an impaired PINK1 (show PINK1 Antibodies)-PARK2-mediated neuroimmunology pathway contributes to septic death.
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.
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
, parkinson juvenile disease protein 2
, parkin variant SV5DEL
, parkin protein
, parkinson protein 2, E3 ubiquitin protein ligase (parkin)