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Product last modified at: 2025-02-11T19:15:09.302Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

CLPP Antibody #14181

Filter:
  • WB
  • IP
Western Blotting Image 1: CLPP Antibody
Western blot analysis of extracts from various cell lines using CLPP Antibody.

To Purchase # 14181

Cat. # Size Qty. Price
14181S 100 µl
$306

Supporting Data

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

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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