Overview

  • Product name

     Human Parkin Matched Antibody Pair Kit
    See all Parkin kits
  • Detection method

    Colorimetric
  • Assay type

    ELISA set
  • Range

    125 pg/ml - 8000 pg/ml
  • Species reactivity

    Reacts with: Human
  • Product overview

    Matched Antibody Pair kit is a titrated unlabeled capture antibody, a titrated biotin-labeled detector and a calibrated protein standard. The Matched Antibody Pair Kit can be used to quantify native and recombinant human Parkin.


    Both capture and detector antibodies are rabbit monoclonal antibodies.


    Optimization of the kit reagents to sample type, immunoassay format or instrumentation may be required. Guidelines for use of this kit in a standard 96-well microplate sandwich ELISA using HRP/TMB system of colorimetric detection is described in this assay procedure for the purposes of quantification.


    Additional protocol information and tips on the use of the Matched Antibody Pair kits for sandwich ELISA can be found on our website.


    For additional information on the performance of the antibody pair used in this kit, please see our equivalent SimpleStep ELISA® (ab212159) which uses the same antibody pair.


    To receive an electronic copy of the Certificate of Analysis, please send an email with "CoA for matched antibody pair kit" in the subject line and the desired product number and lot number in the body of the email.


    Buffer information:
    The capture antibody is glycerol free.
    The detector antibody contains glycerol.

  • Tested applications

    Suitable for: ELISAmore details
  • Platform

    Reagents

Properties

  • Storage instructions

    Store at -20°C. Please refer to protocols.
  • Components 10 x 96 tests 2 x 96 tests
    Human Parkin Capture Antibody 1 x 100µg 1 x 20µg
    Human Parkin Detector Antibody 1 x 25µg 1 x 5µg
    Human Parkin Lyophilized Protein 1 vial 1 vial
  • Research areas

  • 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.
  • 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).
  • Pathway

    Protein modification; protein ubiquitination.
  • 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.
    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 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.
  • Domain

    The ubiquitin-like domain binds the PSMD4 subunit of 26S proteasomes.
  • Post-translational
    modifications

    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.
  • Cellular localization

    Cytoplasm > 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
  • Alternative names

    • AR JP
    • E3 ubiquitin ligase
    • E3 ubiquitin protein ligase parkin
    • E3 ubiquitin-protein ligase parkin
    • FRA6E
    • LPRS 2
    • LPRS2
    • PARK 2
    • Park2
    • Parkin 2
    • Parkinson disease (autosomal recessive juvenile) 2
    • Parkinson disease (autosomal recessive, juvenile) 2, parkin
    • Parkinson disease protein 2
    • Parkinson juvenile disease protein 2
    • Parkinson protein 2 E3 ubiquitin protein ligase
    • Parkinson protein 2, E3 ubiquitin protein ligase (parkin)
    • PDJ
    • PRKN
    • PRKN 2
    • PRKN2
    • PRKN2_HUMAN
    • Ubiquitin E3 ligase PRKN
    see all
  • Database links

Associated products

Applications

Our Abpromise guarantee covers the use of ab217618 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
ELISA Use at an assay dependent concentration.

Images

  • Standard calibration curve. Background subtracted values are graphed.

Protocols

References

ab217618 has not yet been referenced specifically in any publications.

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