Render Target: STATIC
Render Timestamp: 2024-12-06T11:10:01.964Z
Commit: 224419269841c11382c4555dbee545259bf6c379
XML generation date: 2024-08-01 15:26:08.447
Product last modified at: 2024-11-06T13:30:19.113Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

CLPP Antibody #14181

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 28
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    CLPP Antibody recognizes endogenous levels of total CLPP protein.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro263 of human CLPP protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    The proteolytic component, Tetradecameric Peptidase (CLpP), is a hexamer in one of four ATP-dependent mitochondrial proteases (CLpXP). CLPP, one of the proteases, is an endopeptidase that is highly conserved among prokaryotes and eukaryotes, both at the level of amino acid sequence and quaternary structure. The active unit of CLPP is a barrel-shaped tetradecamer, Proteolysis of larger substrates is initiated by caseinolytic peptidase X (CLPX) which unfolds specific protein substrates. The unfolded polypeptide chain translocates into the CLPP proteolytic chamber for protein degradation within the interior chamber of mitochondria (1). Recessive mutations in CLPP cause Perrault Syndrome, a heterogeneous condition characterized by sensorineural hearing loss and ovarian failure (2).

    Mutations in Parkin or PINK1 cause recessively inherited Parkinson’s disease. In healthy mitochondria, PINK1 is rapidly degraded by mitochondrial proteases and the proteasome. Upon mitochondrial depolarization, PINK1 accumulates on the mitochondrial surface, recruits Parkin from the cytosol, and initiates mitophagy. The mitochondrial proteases MPP, PARL, m-AAA and CLPP have been implicated in PINK1 degradation and cleavage (3).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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