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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 Antibodies (180) and PARK2 Proteins (11) and many more products for this protein.
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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 in parallel with Parkin
Maintenance of tissue homeostasis upon reduction of Pink1 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 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 is essential for the mitochondrial translocation of Parkin and for subsequent phosphorylation and activation of Parkin.
Our data indicate that PINK1 and Parkin play an important role in FUS (show FUS ELISA Kits)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (show FUS ELISA Kits) proteinopathy and PINK1/Parkin genes, providing new insights into the pathogenesis of FUS (show FUS ELISA Kits) proteinopathy.
Clu (show CLU ELISA Kits) is upstream of and binds to VCP (show vcp ELISA Kits) in vivo and promotes VCP (show vcp ELISA Kits)-dependent Marf (show MFN2 ELISA Kits) degradation in vitro Marf (show MFN2 ELISA Kits) accumulates in whole muscle lysates of clu (show CLU ELISA Kits)-deficient flies and is destabilized upon Clu (show CLU ELISA Kits) overexpression. Thus, Clu (show CLU ELISA Kits) is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP (show vcp ELISA Kits) for Marf (show MFN2 ELISA Kits) degradation to promote damaged mitochondrial clearance.
Buffy has a role enhancing the loss of parkin and suppressing the loss of Pink1 phenotypes in Drosophila
Parkin-dependent mitophagy suppresses neural neurodegeneration by removing damaged mitochondria.
Thus, the present study indicated that parkin knockout inhibits neural stem cell differentiation by JNK (show MAPK8 ELISA Kits)-dependent proteasomal degradation of p21 (show CDKN1A ELISA Kits).
Parkin hyper-activation by pUb(S57 (show CD81 ELISA Kits)) demonstrates the first PINK1-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 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 ELISA Kits)) and lung cancer.
Here we review the evidence supporting PINK1/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 regulates parkin substrate AIMP2 toxicity by facilitating lysosomal clearance of AIMP2.
Results show that HERC5 mediates covalent ISG15 (show ISG15 ELISA Kits) conjugation to parkin in mammalian cells and that ISG15 (show ISG15 ELISA Kits) is conjugated to the Lys349 and Lys369 residues of parkin. This ISGylation increases the ubiquitin E3 ligase activity of parkin. Also, some familial Parkinson's disease-associated missense mutations of parkin display defective ISGylation.
an impaired PINK1-PARK2-mediated neuroimmunology pathway contributes to septic death.
Melatonin, added together with MPTP or added once MPTP was removed, prevented and recovered, respectively, the parkinsonian phenotype once it was established, restoring gene expression and normal function of the parkin/PINK1/DJ-1/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 ELISA Kits) toxicity.
Park2 deficiency exacerbates ethanol-induced dopaminergic neuron damage through p38 (show CRK ELISA Kits) 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 and PARKIN in this process.
These findings suggest that insufficient mitophagy-mediated PDGFR (show PDGFRB ELISA Kits)/PI3K/AKT (show AKT1 ELISA Kits) 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 ELISA Kits) downregulation or the exogenous expression of normal Parkin restored cytosolic Ca(2 (show CA2 ELISA Kits)+) 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 ELISA Kits) 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)