Use your antibodies-online credentials, if available.
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. 再加上，我们可以发PARK2 抗体 (180) 和 PARK2 蛋白 (11)和数多这个蛋白质的别的产品。
Showing 4 out of 18 products:
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 (显示 FUS ELISA试剂盒)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (显示 FUS ELISA试剂盒) proteinopathy and PINK1/Parkin genes, providing new insights into the pathogenesis of FUS (显示 FUS ELISA试剂盒) proteinopathy.
Clu (显示 CLU ELISA试剂盒) is upstream of and binds to VCP (显示 vcp ELISA试剂盒) in vivo and promotes VCP (显示 vcp ELISA试剂盒)-dependent Marf (显示 MFN2 ELISA试剂盒) degradation in vitro Marf (显示 MFN2 ELISA试剂盒) accumulates in whole muscle lysates of clu (显示 CLU ELISA试剂盒)-deficient flies and is destabilized upon Clu (显示 CLU ELISA试剂盒) overexpression. Thus, Clu (显示 CLU ELISA试剂盒) is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP (显示 vcp ELISA试剂盒) for Marf (显示 MFN2 ELISA试剂盒) 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 (显示 vps35 ELISA试剂盒) 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.
These findings suggest that insufficient mitophagy-mediated PDGFR (显示 PDGFRB ELISA试剂盒)/PI3K/AKT (显示 AKT1 ELISA试剂盒) 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 (显示 MFN2 ELISA试剂盒) downregulation or the exogenous expression of normal Parkin restored cytosolic Ca(2 (显示 CA2 ELISA试剂盒)+) 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 (显示 CRMP1 ELISA试剂盒) to the pathogenesis of sporadic Parkinson's disease (PD). These findings indicate that the SNO (显示 SBNO2 ELISA试剂盒)-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 (显示 CRMP1 ELISA试剂盒)-independent mechanism.
Parkin-overexpressing cells also showed reductions in apoptotic BAX (显示 BAX ELISA试剂盒) translocation to the mitochondria and cytochrome c (显示 CYCS ELISA试剂盒) release to the cytosol
Parkin protects against oxygen-glucose deprivation/reperfusion insult by promoting degradation of Drp1 (显示 CRMP1 ELISA试剂盒).
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.
p62 (显示 GTF2H1 ELISA试剂盒) are subjected to parkin mediated proteasomal degradation
these results unveil a novel functional coupling between Parkin and the CaV2.2 (显示 CACNA1B ELISA试剂盒) 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 (显示 PARL ELISA试剂盒)-PINK1-Parkin system. Findings reveal the sequential adipogenic events directed by PARL (显示 PARL ELISA试剂盒)-PINK1-Parkin system, add more evidence supporting the convergence of pathogenesis leading to neurodegenerative and metabolic disease
These results highlight the combined effects of Parkin and PGC-1alpha (显示 PPARGC1A ELISA试剂盒) in the maintenance of mitochondrial homeostasis in dopaminergic neurons. These two factors synergistically control the quality and function of mitochondria, which is important for the survival of neurons in Parkinson's disease.
Data suggest that inactivation of cytosolic parkin in dopaminergic neurons of the substantia nigra contributes to neurodegeneration in sporadic Parkinson disease. [REVIEW]
we identified a genome-wide significant association involving measures of midface height at 6q26 within an intron of PARK2
PARK2 inactivation connects energy and oxidative stress to Akt activation via redox-mediated inactivation of PTEN by S-nitrosylation to support cell survival under conditions of energy deprivation.
These results suggest that degradation of endogenous APE1 (显示 APEX1 ELISA试剂盒) by Parkin occur when cells are stressed to activate Parkin, and imply a role of Parkin in maintaining the quality of APE1 (显示 APEX1 ELISA试剂盒), and loss of Parkin may contribute to elevated APE1 (显示 APEX1 ELISA试剂盒) levels in glioblastoma.
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
, parkin protein
, parkin variant SV5DEL
, parkinson juvenile disease protein 2