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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. Zusätzlich bieten wir Ihnen PARK2 Antikörper (197) und PARK2 Kits (21) und viele weitere Produktgruppen zu diesem Protein an.
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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 (zeige PINK1 Proteine) in parallel with Parkin
Maintenance of tissue homeostasis upon reduction of Pink1 (zeige PINK1 Proteine) 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 (zeige PINK1 Proteine) 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 (zeige PINK1 Proteine) is essential for the mitochondrial translocation of Parkin and for subsequent phosphorylation and activation of Parkin.
Our data indicate that PINK1 (zeige PINK1 Proteine) and Parkin play an important role in FUS (zeige FUS Proteine)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (zeige FUS Proteine) proteinopathy and PINK1 (zeige PINK1 Proteine)/Parkin genes, providing new insights into the pathogenesis of FUS (zeige FUS Proteine) proteinopathy.
Clu (zeige CLU Proteine) is upstream of and binds to VCP (zeige vcp Proteine) in vivo and promotes VCP (zeige vcp Proteine)-dependent Marf (zeige MFN2 Proteine) degradation in vitro Marf (zeige MFN2 Proteine) accumulates in whole muscle lysates of clu (zeige CLU Proteine)-deficient flies and is destabilized upon Clu (zeige CLU Proteine) overexpression. Thus, Clu (zeige CLU Proteine) is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP (zeige vcp Proteine) for Marf (zeige MFN2 Proteine) degradation to promote damaged mitochondrial clearance.
mitochondrial dysfunction activates the PINK1 (zeige PINK1 Proteine)/Parkin signaling and mitophagy in renal tubular epithelial cells under albumin (zeige ALB Proteine) overload condition.
The authors demonstrate that RABGEF1 (zeige RABGEF1 Proteine), the upstream factor of the endosomal Rab GTPase (zeige RAB6A Proteine) cascade, is recruited to damaged mitochondria via ubiquitin binding downstream of Parkin. RABGEF1 (zeige RABGEF1 Proteine) directs the downstream Rab (zeige HRB Proteine) proteins, RAB5 (zeige RAB5A Proteine) and RAB7A (zeige RAB7A Proteine), to damaged mitochondria, whose associations are further regulated by mitochondrial Rab (zeige HRB Proteine)-GAPs.
DNAJ (zeige DNAJB6 Proteine) proteins keep Parkin C289G mutant protein in a soluble, degradation-competent form.
S-nitrosylated PINK1 (zeige PINK1 Proteine) 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 protein (THAP11) 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.
Melatonin, added together with MPTP (zeige PTPN2 Proteine) or added once MPTP (zeige PTPN2 Proteine) was removed, prevented and recovered, respectively, the parkinsonian phenotype once it was established, restoring gene expression and normal function of the parkin/PINK1 (zeige PINK1 Proteine)/DJ-1 (zeige PARK7 Proteine)/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
PINK1 (zeige PINK1 Proteine) and PARK2 suppress pancreatic tumorigenesis through control of mitochondrial iron-mediated immunometabolism
When fed with iron-supplemented diet, DMT1 (zeige SLC11A2 Proteine)-expressing mice exhibit rather selective accumulation of iron in the substantia nigra but otherwise seem normal. Parkin expression is also enhanced, likely as a neuroprotective response. When DMT1 (zeige SLC11A2 Proteine) is overexpressed against a Parkin null background, the double-mutant mice similarly resisted a disease phenotype when fed with iron or manganese, but greater susceptibility to 6-OHDA.
Bnip3l (zeige BNIP3L Proteine) knockout (bnip3l (zeige BNIP3L Proteine)(-/-)) impaired mitophagy and aggravated cerebral I-R (ischemia-reperfusion) injury in mice, which can be rescued by BNIP3L (zeige BNIP3L Proteine) overexpression. The rescuing effects of BNIP3L (zeige BNIP3L Proteine) 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 (zeige PINK1 Proteine) 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 (zeige SOD1 Proteine) toxicity.
Park2 deficiency exacerbates ethanol-induced dopaminergic neuron damage through p38 (zeige CRK Proteine) 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 (zeige MUL1 Proteine) and PARKIN in this process.
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)