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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 (23) and PARK2 Proteins (8) and many more products for this protein.
Showing 10 out of 191 products:
Human Polyclonal PARK2 Primary Antibody for EIA, IHC (p) - ABIN358990
Kumru, Santamaria, Tolosa, Valldeoriola, Muñoz, Marti, Iranzo: Rapid eye movement sleep behavior disorder in parkinsonism with parkin mutations. in Annals of neurology 2004
Show all 5 references for ABIN358990
Human Monoclonal PARK2 Primary Antibody for IF, WB - ABIN393540
Kägi, Klein, Wood, Schneider, Pramstaller, Tadic, Quinn, van de Warrenburg, Bhatia: Nonmotor symptoms in Parkin gene-related parkinsonism. in Movement disorders : official journal of the Movement Disorder Society 2010
Show all 5 references for ABIN393540
Human Polyclonal PARK2 Primary Antibody for FACS, IF - ABIN390366
West, Kapatos, OFarrell, Gonzalez-de-Chavez, Chiu, Farrer, Maidment: N-myc regulates parkin expression. in The Journal of biological chemistry 2004
Show all 2 references for ABIN390366
Human Polyclonal PARK2 Primary Antibody for FACS, IF - ABIN390365
Wang, Denison, Lai, Philips, Montoya, Kock, Schüle, Klein, Shridhar, Roberts, Smith: Parkin gene alterations in hepatocellular carcinoma. in Genes, chromosomes & cancer 2004
Show all 2 references for ABIN390365
Human Polyclonal PARK2 Primary Antibody for EIA, WB - ABIN358989
Pigullo, De Luca, Barone, Marchese, Bellone, Colosimo, Scaglione, Martinelli, Di Maria, Pizzuti, Abbruzzese, Dallapiccola, Ajmar, Mandich: Mutational analysis of parkin gene by denaturing high-performance liquid chromatography (DHPLC) in essential tremor. in Parkinsonism & related disorders 2004
Show all 2 references for ABIN358989
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
Cow (Bovine) Polyclonal PARK2 Primary Antibody for WB - ABIN372697
Jenner, Dexter, Sian, Schapira, Marsden: Oxidative stress as a cause of nigral cell death in Parkinson's disease and incidental Lewy body disease. The Royal Kings and Queens Parkinson's Disease Research Group. in Annals of neurology 1992
We demonstrate here that vps35 (show vps35 Antibodies) genetically interacts with parkin
Clu (show CLU Antibodies) directly modulates mitochondrial function, and that Clu's function contributes to the PINK1 (show PINK1 Antibodies)-Park pathway of mitochondrial quality control.
Human Mask homolog ANKHD1 (show ANKHD1 Antibodies) may serve as a potential therapeutic target for treating Parkinson disease caused by pink1 (show PINK1 Antibodies)/parkin mutations.
These results indicate that the in vivo rescue is due to restoring CI activity rather than promoting mitophagy Our findings support the emerging view that PINK1 (show PINK1 Antibodies) plays a role in regulating CI activity separate from its role with Parkin in mitophagy
MUL1 (show MUL1 Antibodies) acts in parallel to the PINK1 (show PINK1 Antibodies)/parkin pathway on a shared target mitofusin (show MFN2 Antibodies) to maintain mitochondrial integrity.
Parkin cooperates with PINK1 to promote hnRNP-F/Glo ubiquitination and nRCC mRNA translation.
The loss-of-function mutation in parkin results in defective immune response against bacterial infection. Additionally, parkin mutant larvae showed hypersensitivity against wound regardless of bacterial infection.
data thus support the potential of folic acid in alleviating the behavioural defects, oxidative stress, augmentation of zinc and ATP levels in parkin knock down flies
Parkin phosphorylation by PINK1 (show PINK1 Antibodies) drives Parkin E3 activity. endogenous PINK1 (show PINK1 Antibodies) precisely controls Parkin activity to maintain the mitochondrial function in muscle tissue and the neuronal function in dopaminergic neurons.
Our findings thus suggest that Lon (show LONP1 Antibodies) plays an essential role in regulating the PINK1 (show PINK1 Antibodies)-Parkin pathway by promoting the degradation of PINK1 (show PINK1 Antibodies) in the matrix of healthy mitochondria
A comprehensive analysis of influence of the Parkinson disease-associated genes Parkin and DJ-1 (show PARK7 Antibodies) on neurotransmitter receptor (show GRIN1 Antibodies) expression in mice
Whereas Parkin has been reported to positively regulate the expression of OPA1 (show MED12 Antibodies) through NEMO (show IKBKG Antibodies), herein we found that PARK2 overexpression did not modify the expression of OPA1 (show MED12 Antibodies).
In mouse hearts Parkin functions as a stress-induced and developmentally-programmed facilitator of cardiomyocyte mitochondrial turnover. (Review)
findings support the notion that BAG2 (show BAG2 Antibodies) is an upstream regulator of the PINK1 (show PINK1 Antibodies)/PARKIN signaling pathway.
The PINK1 (show PINK1 Antibodies)-Parkin pathway is activated in response to metabolic stress
Overexpressed human wild type alpha-synuclein (show SNCA Antibodies) in the substantia nigra was phosphorylated at Ser (show SIGLEC1 Antibodies) 129 significantly more in parkin knockout mice, though the total alpha synuclein (show SNCA Antibodies) levels were the same as in wild type mice.
analysis of two types of mitophagy, a DNM1L (show DNM1L Antibodies)-dependent pathway and a PARK2-dependent pathway
FBXW8 (show FBXW8 Antibodies) and PARK2 are sequestrated into insolubility by ATXN2 (show ATXN2 Antibodies) PolyQ expansions, but only FBXW8 (show FBXW8 Antibodies) expression is dysregulated
PARK2 function where damaged mitochondria are targeted for degradation via a PARK2/PINK1 (show PINK1 Antibodies)-mediated mechanism.
instead of transcriptional reprogramming, fetal cardiomyocyte mitochondria undergo perinatal Parkin-mediated mitophagy and replacement by mature adult mitochondria. Mitophagic mitochondrial removal underlies developmental cardiomyocyte mitochondrial plasticity and metabolic transitioning of perinatal hearts.
Fibroblasts isolated from skin biopsy specimens from patients with genetic forms of Parkinson's disease, carriers of mutations in LRRK2 (show LRRK2 Antibodies) and PARK2 genes, and from a healthy volunteer were reprogrammed into induced pluripotent stem cells.
PARK2 mutant neuroprogenitors show increased cytotoxicity with copper (Cu) and cadmium (Cd) exposure, and a substantial increase in mitochondrial fragmentation, initial ROS (show ROS1 Antibodies) generation, and loss of mitochondrial membrane potential following Cu exposure.
These studies provide valuable insight into the roles, and cellular hierarchy, of distinct phosphorylation events in parkin activation, and profiles mutations in Parkinson's patients.
UBL domain specifically interacts with the R1 domain and negatively regulates Parkin E3 ligase activity.
A recent report, solving the structure of a Parkin-phosphoubiquitin complex, greatly advances the understanding of the Parkin activation mechanism.
Study shows that heterozygous carriers of copy number variants affecting exons of PARK2 have greater risk of Parkinson's disease than non-carriers.
A role was established for Parkin in regulating the endo-lysomal pathway.
pathogenic PINK1 (show PINK1 Antibodies) mutants which are not cleaved by PARL (show PARL Antibodies) affect PINK1 (show PINK1 Antibodies) kinase activity and the ability to induce PARK2-mediated mitophagy.
Maintenance of appropriate mitochondrial HSD17B10 (show HSD17B10 Antibodies) levels is one of mechanisms by which PARK2 preserves mitochondrial quality. The loss of this protective mechanism may contribute to mitochondrial dysfunction and neuronal degeneration in Parkinson Disease
Epistatic SNP-SNP interactions involving PARK2 and cytokine genes provide an additive risk towards leprosy susceptibility.
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