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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 Kits (22) and PARK2 Proteins (12) and many more products for this protein.
Showing 10 out of 192 products:
Human Polyclonal PARK2 Primary Antibody for ELISA, WB - ABIN251684
La Cognata, Iemmolo, DAgata, Scuderi, Drago, Zappia, Cavallaro: Increasing the Coding Potential of Genomes Through Alternative Splicing: The Case of PARK2 Gene. in Current genomics 2014
Show all 2 Pubmed References
Human Polyclonal PARK2 Primary Antibody for IHC (p), IP - ABIN269703
Scuderi, La Cognata, Drago, Cavallaro, DAgata: Alternative splicing generates different parkin protein isoforms: evidences in human, rat, and mouse brain. in BioMed research international 2014
Show all 2 Pubmed References
Human Polyclonal PARK2 Primary Antibody for IF (p), IHC (p) - ABIN735578
Li, Zhang, Wang, Liu, Yang, Liu, Lu: Neuroprotective effects of extract of Acanthopanax senticosus harms on SH-SY5Y cells overexpressing wild-type or A53T mutant ?-synuclein. in Phytomedicine : international journal of phytotherapy and phytopharmacology 2014
Human Monoclonal PARK2 Primary Antibody for IF, WB - ABIN2476069
Ostby: [Fredrik Nightingale fellows]. in Journalen sykepleien 1990
Show all 2 Pubmed References
Human Monoclonal PARK2 Primary Antibody for IF, ELISA - ABIN562106
Brody, Taylor, Wilson, Delatycki, Lockhart: Regional and cellular localisation of Parkin co-regulated gene in developing and adult mouse brain. in Brain research 2008
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 (show PINK1 Antibodies) in parallel with Parkin
Maintenance of tissue homeostasis upon reduction of Pink1 (show PINK1 Antibodies) 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 Antibodies) 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 Antibodies) is essential for the mitochondrial translocation of Parkin and for subsequent phosphorylation and activation of Parkin.
Our data indicate that PINK1 (show PINK1 Antibodies) and Parkin play an important role in FUS (show FUS Antibodies)-induced neurodegeneration. This study has uncovered a previously unknown link between FUS (show FUS Antibodies) proteinopathy and PINK1 (show PINK1 Antibodies)/Parkin genes, providing new insights into the pathogenesis of FUS (show FUS Antibodies) proteinopathy.
Clu (show CLU Antibodies) is upstream of and binds to VCP (show vcp Antibodies) in vivo and promotes VCP (show vcp Antibodies)-dependent Marf (show MFN2 Antibodies) degradation in vitro Marf (show MFN2 Antibodies) accumulates in whole muscle lysates of clu (show CLU Antibodies)-deficient flies and is destabilized upon Clu (show CLU Antibodies) overexpression. Thus, Clu (show CLU Antibodies) is essential for mitochondrial homeostasis and functions in concert with Parkin and VCP (show vcp Antibodies) for Marf (show MFN2 Antibodies) degradation to promote damaged mitochondrial clearance.
Studies indicate a functional PTEN-induced putative kinase 1)(PINK1 (show PINK1 Antibodies))/E3 ubiquitin protein ligase (parkin) mitophagy pathway in neurons [Review].
parkin deficiency induces synaptotagmin-11 (show SYT11 Antibodies) accumulation and PD-like neurotoxicity in mouse models, which is reversed by SYT11 (show SYT11 Antibodies) knockdown in the SNpc or knockout of SYT11 (show SYT11 Antibodies) restricted to dopaminergic neuron
Parkin expression is inversely correlated with HIF-1alpha (show HIF1A Antibodies) expression and metastasis in breast cancer. Results reveal an important mechanism for Parkin in tumor suppression and HIF-1alpha (show HIF1A Antibodies) regulation.
mitochondrial dysfunction activates the PINK1 (show PINK1 Antibodies)/Parkin signaling and mitophagy in renal tubular epithelial cells under albumin (show ALB Antibodies) overload condition.
The authors demonstrate that RABGEF1 (show RABGEF1 Antibodies), the upstream factor of the endosomal Rab GTPase (show RAB6A Antibodies) cascade, is recruited to damaged mitochondria via ubiquitin binding downstream of Parkin. RABGEF1 (show RABGEF1 Antibodies) directs the downstream Rab (show HRB Antibodies) proteins, RAB5 (show RAB5A Antibodies) and RAB7A (show RAB7A Antibodies), to damaged mitochondria, whose associations are further regulated by mitochondrial Rab (show HRB Antibodies)-GAPs.
DNAJ (show DNAJB6 Antibodies) proteins keep Parkin C289G mutant protein in a soluble, degradation-competent form.
S-nitrosylated PINK1 (show PINK1 Antibodies) 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 (show THAP11 Antibodies) protein (THAP11 (show THAP11 Antibodies)) 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.
Melatonin, added together with MPTP (show PTPN2 Antibodies) or added once MPTP (show PTPN2 Antibodies) 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 Antibodies)/DJ-1 (show PARK7 Antibodies)/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
Overexpression of parkin resulted in a significant reduction of total-eNOS (show NOS3 Antibodies) and p-eNOS (show NOS3 Antibodies) in parallel with the downregulation of ERRalpha (show ESRRA Antibodies) (a regulator of eNOS (show NOS3 Antibodies)) protein and the enhancement of ERRalpha (show ESRRA Antibodies) ubiquitination.
Parkin mice carrying a deletion in exon 3 display impairments in the main pathway responsible for maintaining BH4 levels in the CNS, an essential cofactor for dopamine synthesis, under inflammatory conditions. Concomitant to this alteration, striatum cells do not upregulate BDNF (show BDNF Antibodies) to confer neuroprotection in LPS (show TLR4 Antibodies)-exposed mice, displaying an increased number of mitochondria of smaller size with perinuclear clustering.
the results indicate that PICK1 (show PICK1 Antibodies) is a potent inhibitor of Parkin, and the reduction of PICK1 (show PICK1 Antibodies) enhances the protective effect of Parkin.
PINK1 (show PINK1 Antibodies) and PARK2 suppress pancreatic tumorigenesis through control of mitochondrial iron-mediated immunometabolism
When fed with iron-supplemented diet, DMT1 (show SLC11A2 Antibodies)-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 (show SLC11A2 Antibodies) 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 (show BNIP3L Antibodies) knockout (bnip3l (show BNIP3L Antibodies)(-/-)) impaired mitophagy and aggravated cerebral I-R (ischemia-reperfusion) injury in mice, which can be rescued by BNIP3L (show BNIP3L Antibodies) overexpression. The rescuing effects of BNIP3L (show BNIP3L Antibodies) 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 (show PINK1 Antibodies) 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 (show SOD1 Antibodies) toxicity.
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)