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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 Kits (19) and many more products for this protein.
Showing 10 out of 11 products:
Maintenance of tissue homeostasis upon reduction of Pink1 (show PINK1 Proteins) 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 Proteins) 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 Proteins) is essential for the mitochondrial translocation of Parkin and for subsequent phosphorylation and activation of Parkin.
Our data indicate that PINK1 (show PINK1 Proteins) and Parkin play an important role in FUS (show FUS Proteins)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (show FUS Proteins) proteinopathy and PINK1 (show PINK1 Proteins)/Parkin genes, providing new insights into the pathogenesis of FUS (show FUS Proteins) proteinopathy.
Clu (show CLU Proteins) is upstream of and binds to VCP (show vcp Proteins) in vivo and promotes VCP (show vcp Proteins)-dependent Marf (show MFN2 Proteins) degradation in vitro Marf (show MFN2 Proteins) accumulates in whole muscle lysates of clu (show CLU Proteins)-deficient flies and is destabilized upon Clu (show CLU Proteins) overexpression. Thus, Clu (show CLU Proteins) is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP (show vcp Proteins) for Marf (show MFN2 Proteins) degradation to promote damaged mitochondrial clearance.
Buffy has a role enhancing the loss of parkin and suppressing the loss of Pink1 (show PINK1 Proteins) phenotypes in Drosophila
Parkin-dependent mitophagy suppresses neural neurodegeneration by removing damaged mitochondria.
We demonstrate here that vps35 (show vps35 Proteins) genetically interacts with parkin
Clu (show CLU Proteins) directly modulates mitochondrial function, and that Clu's function contributes to the PINK1 (show PINK1 Proteins)-Park pathway of mitochondrial quality control.
VPS35 (show vps35 Proteins) regulates parkin substrate AIMP2 (show AIMP2 Proteins) toxicity by facilitating lysosomal clearance of AIMP2 (show AIMP2 Proteins).
Results show that HERC5 (show HERC5 Proteins) mediates covalent ISG15 (show ISG15 Proteins) conjugation to parkin in mammalian cells and that ISG15 (show ISG15 Proteins) 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 (show PINK1 Proteins)-PARK2-mediated neuroimmunology pathway contributes to septic death.
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 (show PINK1 Proteins), and DJ-1 (show PARK7 Proteins) 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 Proteins) 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 (show ROS1 Proteins) may act as a trigger for the induction of Parkin/PINK1 (show PINK1 Proteins)-dependent mitophagy.
Melatonin, added together with MPTP (show PTPN2 Proteins) or added once MPTP (show PTPN2 Proteins) 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 Proteins)/DJ-1 (show PARK7 Proteins)/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
Park2 deficiency exacerbates ethanol-induced dopaminergic neuron damage through p38 (show CRK Proteins) 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 Proteins) and PARKIN in this process.
These findings suggest that insufficient mitophagy-mediated PDGFR (show PDGFRB Proteins)/PI3K/AKT (show AKT1 Proteins) 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 Proteins) downregulation or the exogenous expression of normal Parkin restored cytosolic Ca(2 (show CA2 Proteins)+) 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 Proteins) 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.
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-independent mechanism.
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)