Typical Testing Data/Standard Curve (for reference only)
Mouse Parkinson disease 2/parkin ELISA Kit | Park2 elisa kit
Mouse Parkinson disease 2/parkin ELISA Kit
Typical Testing Data/Standard Curve (for reference only)
Typical Testing Data/Standard Curve (for reference only)
Principle of the Assay: PARK2 ELISA kit applies the competitive enzyme immunoassay technique utilizing a polyclonal anti-PARK2 antibody and an PARK2-HRP conjugate. The assay sample and buffer are incubated together with PARK2-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the PARK2 concentration since PARK2 from samples and PARK2-HRP conjugate compete for the anti-PARK2 antibody binding site. Since the number of sites is limited, as more sites are occupied by PARK2 from the sample, fewer sites are left to bind PARK2-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The PARK2 concentration in each sample is interpolated from this standard curve.
NCBI and Uniprot Product Information
NCBI Description
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. [provided by RefSeq]
Uniprot Description
Function: Functions within a multiprotein E3 ubiquitin ligase complex, catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins, such as BCL2, SYT11, CCNE1, GPR37, STUB1, a 22 kDa O-linked glycosylated isoform of SNCAIP, SEPT5, ZNF746 and AIMP2. Mediates monoubiquitination as well as 'Lys-48'-linked and 'Lys-63'-linked polyubiquitination of substrates depending on the context. Participates in the removal and/or detoxification of abnormally folded or damaged protein by mediating 'Lys-63'-linked polyubiquitination of misfolded proteins such as PARK7: 'Lys-63'-linked polyubiquitinated misfolded proteins are then recognized by HDAC6, leading to their recruitment to aggresomes, followed by degradation. Mediates 'Lys-63'-linked polyubiquitination of SNCAIP, possibly playing a role in Lewy-body formation. Mediates monoubiquitination of BCL2, thereby acting as a positive regulator of autophagy. Promotes the autophagic degradation of dysfunctional depolarized mitochondria. Mediates 'Lys-48'-linked polyubiquitination of ZNF746, followed by degradation of ZNF746 by the proteasome; possibly playing a role in role in regulation of neuron death. Limits the production of reactive oxygen species (ROS). 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. Ref.10 Ref.11 Ref.20 Ref.22 Ref.24 Ref.26 Ref.27 Ref.31 Ref.32 Ref.33 Ref.35 Ref.36 Ref.37 Ref.38
Pathway: Protein modification; protein ubiquitination.
Subunit structure: Forms an E3 ubiquitin ligase complex with UBE2L3 or UBE2L6. Mediates 'Lys-63'-linked polyubiquitination by associating with UBE2V1. 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. Interacts (via first RING-type domain) with AIMP2 (via N-terminus). Interacts with PSMA7 and RNF41. Interacts with PINK1. Ref.12 Ref.14 Ref.17 Ref.18 Ref.19 Ref.20 Ref.25 Ref.26 Ref.27 Ref.28 Ref.29 Ref.30 Ref.33 Ref.34 Ref.35 Ref.36 Ref.37 Ref.38 Ref.39
Subcellular location: Cytoplasm › cytosol. Nucleus. Endoplasmic reticulum. Mitochondrion. Note: Mainly localizes in the cytosol. Co-localizes with SYT11 in neutrites. Co-localizes with SNCAIP in brainstem Lewy bodies. Relocates to dysfunctional mitochondria that have lost the mitochondial membrane potential; recruitement to mitochondria is PINK1-dependent. Ref.2 Ref.9 Ref.15 Ref.30 Ref.31 Ref.32 Ref.35 Ref.36
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. Found in serum (at protein level). Ref.2
Domain: The ubiquitin-like domain binds the PSMD4 subunit of 26S proteasomes. Ref.16
Post-translational modification: Auto-ubiquitinates in an E2-dependent manner leading to its own degradation. Also polyubiquitinated by RNF41 for proteasomal 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.
Involvement in disease: Defects in PARK2 are a cause of Parkinson disease (PARK) [
MIM:168600]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease 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. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features. Ref.1 Ref.11 Ref.14 Ref.15 Ref.18 Ref.35 Ref.36 Ref.37 Ref.40 Ref.42 Ref.44 Ref.46 Ref.48 Ref.49 Ref.50 Ref.51 Ref.52 Ref.54 Ref.55 Ref.56 Ref.57 Ref.58 Ref.59 Ref.60 Ref.62Defects in PARK2 are the cause of Parkinson disease type 2 (PARK2) [
MIM:600116]; also known as early-onset parkinsonism with diurnal fluctuation (EPDF) or autosomal recessive juvenile Parkinson disease (PDJ). A neurodegenerative disorder characterized by bradykinesia, rigidity, postural instability, tremor, and onset usually befor 40. It differs from classic Parkinson disease by early DOPA-induced dyskinesia, diurnal fluctuation of the symptoms, sleep benefit, dystonia and hyper-reflexia. Dementia is absent. Pathologically, 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. Ref.1 Ref.14 Ref.35 Ref.40 Ref.42 Ref.44 Ref.46 Ref.50 Ref.51 Ref.54Note=Defects in PARK2 may be involved in the development and/or progression of ovarian cancer.
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.Members of the RBR family are atypical E3 ligases. They interact with the E2 conjugating enzyme UBE2L3 and function like HECT-type E3 enzymes: they bind E2s via the first RING domain, but require an obligate trans-thiolation step during the ubiquitin transfer, requiring a conserved cysteine residue in the second RING domain (Ref.38).
Sequence similarities: Belongs to the RBR family. Parkin subfamily.Contains 1 IBR-type zinc finger.Contains 2 RING-type zinc fingers.Contains 1 ubiquitin-like domain.
Research Articles on Park2
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Product Notes
The Mouse Park2 park2 (Catalog #AAA723678) is an ELISA Kit and is intended for research purposes only. The product is available for immediate purchase. The AAA723678 ELISA Kit recognizes Mouse Park2. It is sometimes possible for the material contained within the vial of "Parkinson disease 2/parkin, ELISA Kit" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.Precautions
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