Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal to Parkin - BSA and Azide free (Detector)
- Suitable for: Sandwich ELISA
- Reacts with: Human
Product nameAnti-Parkin antibody - BSA and Azide free (Detector)
See all Parkin primary antibodies
DescriptionRabbit monoclonal to Parkin - BSA and Azide free (Detector)
Tested applicationsSuitable for: Sandwich ELISAmore details
Species reactivityReacts with: Human
ab242818 is a BSA and Azide Free antibody supplied in an unconjugated format and it is suitable for sandwich ELISAs to quantify Human Parkin. The recommended pair for sandwich ELISA is:
Capture: ab242571, Human Parkin Capture Antibody (unconjugated)
Detector: ab242818, Human Parkin Detector Antibody (unconjugated)
The reference range value is 125 - 8000 pg/ml.
The recommended antibody orientation is based on internal optimization for ELISA-based assays. Antibody orientation is assay dependent and needs to be optimized for each assay type. Please note that the range provided for this antibody is only an estimation based on the performance of the product using the recommended antibody pair. Performance of the antibody pair will depend on the specific characteristics of your assay. We guarantee the product works in sandwich ELISA, but we do not guarantee the sensitivity or dynamic range of the antibody in your assay.
Our carrier-free formats are supplied in a buffer free of BSA, sodium azide and glycerol for higher conjugation efficiency. The antibodies are provided at an approximate concentration of 1 mg/ml as measured by the protein A280 method. Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with <1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
This product is a recombinant monoclonal antibody, which offers several advantages including:
-High batch-to-batch consistency and reproducibility
-Improved sensitivity and specificity
-Long-term security of supply
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
Storage instructionsShipped at 4°C. Store at +4°C.
Storage bufferConstituent: 100% PBS
Concentration information loading...
sELISA pair antibody
Our Abpromise guarantee covers the use of ab242818 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Sandwich ELISA||Use at an assay dependent concentration. Can be paired for Sandwich ELISA with Rabbit monoclonal to Parkin - BSA and Azide free (Capture) (ab242571).|
FunctionFunctions 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.
Tissue specificityHighly 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).
PathwayProtein modification; protein ubiquitination.
Involvement in diseaseDefects 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.
Defects 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.
Note=Defects in PARK2 may be involved in the development and/or progression of ovarian cancer.
Sequence similaritiesBelongs to the RBR family. Parkin subfamily.
Contains 1 IBR-type zinc finger.
Contains 2 RING-type zinc fingers.
Contains 1 ubiquitin-like domain.
DomainThe ubiquitin-like domain binds the PSMD4 subunit of 26S proteasomes.
modificationsAuto-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.
Cellular localizationCytoplasm > cytosol. Nucleus. Endoplasmic reticulum. Mitochondrion. 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.
- Information by UniProt
- AR JP antibody
- E3 ubiquitin ligase antibody
- E3 ubiquitin protein ligase parkin antibody
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab242818 has not yet been referenced specifically in any publications.