05-882 | Anti-Parkin Antibody, clone PRK8

100 µL  
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      Key Spec Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      H, MIP, WB, ICC, IHCMAscitesMonoclonal Antibody
      Catalogue Number05-882
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-Parkin Antibody, clone PRK8
      Product Information
      ApplicationAnti-Parkin Antibody, clone PRK8 detects level of Parkin & has been published & validated for use in IP, WB, IC, IH.
      Key Applications
      • Immunoprecipitation
      • Western Blotting
      • Immunocytochemistry
      • Immunohistochemistry
      Biological Information
      ImmunogenFull length recombinant human Parkin. Epitope has been mapped to the second ring domain (aa 399-465)
      Cloneclone PRK8
      Species Reactivity
      • Human
      • Mouse
      Antibody TypeMonoclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryThe 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.
      Gene Symbol
      • PARK2
      • PDJ
      • Parkin
      • AR-JP
      • PRKN
      • LPRS2
      • parkin
      Purification MethodAscites
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: O60260 # Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins. These substrates include SYT11, CCNE1, GPR37, STUB1, a 22 kDa O-linked glycosylated isoform of SNCAIP and SEPT5. May play a more general role in the ubiquitin proteasomal pathway by participating in the removal and/or detoxification of abnormally folded or damaged protein. Loss of this ubiquitin ligase activity appears to be the mechanism underlying pathogenesis of PARK2. May protect neurons against alpha synuclein toxicity, proteasomal dysfunction, GPR37 accumulation, and kainate-induced excitotoxicity. May play a role in controlling neurotransmitter trafficking at the presynaptic terminal and in calcium-dependent exocytosis. Regulates cyclin E during neuronal apoptosis. May represent a tumor suppressor gene.
      SIZE: 465 amino acids; 51641 Da
      SUBUNIT: Forms an E3 ubiquitin ligase complex with UBE2L3 or UBE2L6. Part of a SCF-like complex, consisting of PARK2, CUL1 and FBXW7. Interacts with SNCAIP. Binds to the C2A and C2B domains of SYT11. Interacts and regulates the turnover of SEPT5. Part of a complex, including STUB1, HSP70 and GPR37. The amount of STUB1 in the complex increases during ER stress. STUB1 promotes the dissociation of HSP70 from PARK2 and GPR37, thus facilitating PARK2-mediated GPR37 ubiquitination. HSP70 transiently associates with unfolded GPR37 and inhibits the E3 activity of PARK2, whereas, STUB1 enhances the E3 activity of PARK2 through promotion of dissociation of HSP70 from PARK2-GPR37 complexes. Interacts with PSMD4 and PACRG. Interacts with LRRK2. Interacts with RANBP2. Interacts with SUMO1 but not SUMO2, which promotes nuclear localization and autoubiquitination.
      SUBCELLULAR LOCATION: Cytoplasm. Note=Co-localizes with STY11 in neutrites. Co-localizes with SNCAIP in brainstem Lewy bodies. Nucleus.
      TISSUE SPECIFICITY: Highly expressed in the brain including the substantia nigra. Expressed in heart, testis and skeletal muscle. Expression is down-regulated or absent in tumor biopsies, and absent in the brain of PARK2 patients. Overexpression protects dopamine neurons from kainate-mediated apoptosis.
      DOMAIN: SwissProt: O60260 The ubiquitin-like domain binds the PSMD4 subunit of 26S proteasomes.
      PTM: Auto-ubiquitinates in an E2-dependent manner leading to its own degradation. & S-nitrosylated. The inhibition of PARK2 ubiquitin E3 ligase activity by S-nitrosylation could contribute to the degenerative process in PD by impairing the ubiquitination of PARK2 substrates.
      DISEASE: SwissProt: O60260 # Defects in PARK2 are a cause of Parkinson disease (PD) [MIM:168600]. PD is a complex, multifactorial disorder that typically manifests after the age of 50 years, although early- onset cases (before 50 years) are known. PD generally arises as a sporadic condition but is occasionally inherited as a simple mendelian trait. Although sporadic and familial PD are very similar, inherited forms of the disease usually begin at earlier ages and are associated with atypical clinical features. PD is characterized by bradykinesia, resting tremor, muscular rigidity and postural instability, as well as by a clinically significant response to treatment with levodopa. The pathology of PD involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain. & Defects in PARK2 are the cause of autosomal recessive early onset Parkinson disease 2 (PARK2) [MIM:600116]; also known as early-onset parkinsonism with diurnal fluctuation (EPDF) or autosomal recessive juvenile Parkinson disease (PDJ). PARK2 is symptomatically different in several aspects from idiopathic Parkinson disease, although classic symptoms such as bradykinesia, rigidity and tremor are present. Additional clinical features include early DOPA-induced dyskinesia, diurnal fluctuation of the symptoms, sleep benefit, dystonia and hyper-reflexia. PARK2 is usually characterized by onset before 40, with a mean age at onset of 23.2 years. Pathologically, PARK2 patients show loss of dopaminergic neurons in the substantia nigra, similar to that seen in Parkinson disease; however, Lewy bodies (intraneuronal accumulations of aggregated proteins) are absent. & Defects in PARK2 may be involved in the development and/or progression of ovarian cancer.
      SIMILARITY: Contains 2 IBR-type zinc fingers. & Contains 2 RING-type zinc fingers. & Contains 1 ubiquitin-like domain.
      MISCELLANEOUS: The parkin locus (PRKN), adjacent to the 6q telomere is hyper-recombinable and lies within FRA6E, the third most common fragile site in tumor tissue.
      Molecular Weight52kDa. May be observed as a doublet at 52 and 46kDa
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality Assuranceroutinely evaluated by immunoblot on RIPA lysates from HEK293 cells
      Usage Statement
      • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
      Storage and Shipping Information
      Storage ConditionsStable for 2 years at -20°C from date of shipment
      Packaging Information
      Material Size100 µL
      Transport Information
      Supplemental Information




      Safety Data Sheet (SDS) 

      Certificates of Analysis

      TitleLot Number
      Anti-Parkin, clone PRK8 mouse monoclonal IgG2b) - 2115546 2115546
      Anti-Parkin, clone PRK8 mouse monoclonal IgG2b) - 2142166 2142166
      Anti-Parkin, clone PRK8 (mouse monoclonal IgG2b) 2918954
      Anti-Parkin, clone PRK8 (mouse monoclonal IgG2b) - 2066010 2066010
      Anti-Parkin, clone PRK8 (mouse monoclonal IgG2b) - 2073581 2073581
      Anti-Parkin, clone PRK8 - 2070834 2070834
      Anti-Parkin, clone PRK8 - 30300 30300
      Anti-Parkin, clone PRK8 mouse monoclonal IgG2b) 3066182
      Anti-Parkin, clone PRK8 mouse monoclonal IgG2b) - 2161121 2161121
      Anti-Parkin, clone PRK8 mouse monoclonal IgG2b) - 2325089 2325089


      Reference overviewPub Med ID
      Mitochondrial fission is required for cardiomyocyte hypertrophy mediated by a Ca2+-calcineurin signaling pathway.
      Pennanen, C; Parra, V; López-Crisosto, C; Morales, PE; Del Campo, A; Gutierrez, T; Rivera-Mejías, P; Kuzmicic, J; Chiong, M; Zorzano, A; Rothermel, BA; Lavandero, S
      Journal of cell science  127  2659-71  2014

      Show Abstract
      24777478 24777478
      Pathogenetic mechanisms of parkin in Parkinson's disease.
      Hattori, Nobutaka and Mizuno, Yoshikuni
      Lancet, 364: 722-4 (2004)  2004

      Show Abstract
      15325839 15325839
      Ubiquitin, proteasome and parkin.
      Tanaka, Keiji, et al.
      Biochim. Biophys. Acta, 1695: 235-47 (2004)  2004

      Show Abstract
      15571819 15571819
      Genotype-phenotype correlation: familial Parkinson disease.
      Mori, Hideo, et al.
      Neuropathology, 23: 90-4 (2003)  2003

      Show Abstract
      12722931 12722931
      Are ubiquitination pathways central to Parkinson's disease?
      Giasson, Benoit I and Lee, Virginia M-Y
      Cell, 114: 1-8 (2003)  2003

      Show Abstract
      12859888 12859888
      Molecular pathways of neurodegeneration in Parkinson's disease.
      Dawson, Ted M and Dawson, Valina L
      Science, 302: 819-22 (2003)  2003

      Show Abstract
      14593166 14593166

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      Life Science Research > Antibodies and Assays > Primary Antibodies