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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 (21) and PARK2 Proteins (12) and many more products for this protein.
Showing 10 out of 194 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
Show all 4 Pubmed References
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, WB - ABIN2476069
Ostby: [Fredrik Nightingale fellows]. in Journalen sykepleien 1990
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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
Loss of parkin is associated with nuclear clustering and morphology defects in larval muscles and thus developing aortic aneurysms.
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.
S-nitrosylated PINK1 (show PINK1 Antibodies) decreases Parkin translocation to mitochondrial membranes
Parkinsonism associated with Parkin gene mutation is one of the most common familial forms of Parkinson Disease, which is characterized by early onset of symptoms, slow progression, elective dopaminergic neuronal loss and the absence of Lewy bodies.
A transcriptional repressor network including THAP domain containing 11 (show THAP11 Antibodies) protein (THAP11 (show THAP11 Antibodies)) was identified and negatively regulates endogenous PARKIN abundance.
Study explored the role of parkin proteins in Parkinson's disease (PD) neurodegeneration by analyzing their expression profile in an in vitro model exposed to divers neurotoxins. Results showed that up- or down-regulation of specific splice isoforms may be a direct effect of toxin exposure. Moreover, the isoforms may exert different actions in neurodegeneration via modulation of different molecular pathways.
Mutations in the PARK2 gene were detected in four of the six tested families with a history of early-onset Parkinson disease.
This study showed that the heterozygous Parkin mutation carriers show subtle motor abnormalities when a detailed, specialized motor examination is applied and compared to mutation-negative matched control subjects.
The methylation of SNCA and PARK2 promoter regions were significantly lower in early-onset Parkinson's disease patients compared to control group. Methylation status of the SNCA might be associated with positive family history of Parkinson's disease.
Show that the C-terminal GTPase of the Parkin primary substrates Miro1 and Miro2 are necessary and sufficient for efficient ubiquitination. We present several new X-ray crystal structures of both Miro1 and Miro2 that reveal substrate recognition and ubiquitin transfer to be specific to particular protein domains and lysine residues.
This study showed that the manganese exposure among smelters may lead to a reduced expression of PARK2.
parkin-dependent targeting of misregulated BAX (show BAX Antibodies) on the mitochondria provides substantial protection against BAX (show BAX Antibodies) apoptotic activity.
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
Bnip3l (show BNIP3L Antibodies) knockout (bnip3l (show BNIP3L Antibodies)(-/-)) impaired mitophagy and aggravated cerebral I-R (ischemia-reperfusion) injury in mice, which can be rescued by BNIP3L (show BNIP3L Antibodies) overexpression. The rescuing effects of BNIP3L (show BNIP3L Antibodies) overexpression can be observed in park2(-/-) mice, which showed mitophagy deficiency after I-R.
Parkin acts as a regulator of microtubule system during neuronal aging.
The expression of PINK1 (show PINK1 Antibodies) and Parkin were elevated in white adipose tissue in obese mice.
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
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)