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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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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.
We demonstrate here that vps35 (show vps35 ELISA Kits) genetically interacts with parkin
Clu directly modulates mitochondrial function, and that Clu's function contributes to the PINK1-Park pathway of mitochondrial quality control.
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.
an impaired PINK1-PARK2-mediated neuroimmunology pathway contributes to septic death.
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 (show SBNO2 ELISA Kits)-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 ELISA Kits)-independent mechanism.
Parkin-overexpressing cells also showed reductions in apoptotic BAX (show BAX ELISA Kits) translocation to the mitochondria and cytochrome c (show CYCS ELISA Kits) release to the cytosol
Parkin protects against oxygen-glucose deprivation/reperfusion insult by promoting degradation of Drp1 (show CRMP1 ELISA Kits).
The identification of PINK1 and Parkin as suppressors of an immune-response-eliciting pathway provoked by inflammation suggests new insights into Parkinson's disease pathology.
This work provided strong new evidence that PARK2 participates to the regulatory networks associated with oxidative phosphorylation and suggested that PARK2 genetic variations could act as a trans regulator of OXPHOS gene macrophage expression in humans.
REVIEW: role of parkin in modulating excitatory and dopaminergic synapse functions
The effects of variants in the Parkin, PINK1, and DJ-1 (show PARK7 ELISA Kits) genes along with evidence for their pathogenicity have been summarized. (Review)
Parkin is a potential link between melanoma and Parkinson's disease
these results unveil a novel functional coupling between Parkin and the CaV2.2 (show CACNA1B ELISA Kits) channels.
These results demonstrate the feasibility of using UbFluor for quantitative studies of the biochemistry of RBR E3s and for high-throughput screening of small-molecule activators or inhibitors of PARKIN and other RBR E3 ligases.
data suggest that ROS may act as a trigger for the induction of Parkin/PINK1-dependent mitophagy.
The proportions of some phospholipids and glycosphingolipids were altered in the lipid profiles of parkin-mutant skin fibroblasts obtained from Parkinson disease patients.
Adipogenic process can be dissected into 3 stages according to the participation of PARL (show PARL ELISA Kits)-PINK1-Parkin system. Findings reveal the sequential adipogenic events directed by PARL (show PARL ELISA Kits)-PINK1-Parkin system, add more evidence supporting the convergence of pathogenesis leading to neurodegenerative and metabolic disease
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
, parkinson juvenile disease protein 2
, parkin variant SV5DEL
, parkin protein
, parkinson protein 2, E3 ubiquitin protein ligase (parkin)