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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

CLIC1 (D7D6H) Rabbit mAb #53424

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 22
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    CLIC1 (D7D6H) Rabbit mAb recognizes endogenous levels of total CLIC1 protein.


    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu234 of human CLIC1 protein.

    Background

    Chloride intracellular channel (CLIC) proteins belong to a family of highly conserved transport proteins found as both soluble and membrane-bound forms (1). Although CLIC proteins have putative, selective chloride ion channel activity, they are structural homologs to members of the glutathione-S-transferase protein superfamily and are likewise regulated by redox status (2). CLIC proteins are distinct from other ion channels in that they are found as both soluble and integral membrane forms, and their form determines their function (3-6). Chloride intracellular channel proteins are ubiquitously expressed in numerous tissue types and are involved in diverse biological functions (1,2).
    CLIC1 is a member of the CLIC protein family. It is ubiquitously expressed in many tissues and organs (7). CLIC1 is overexpressed in multiple tumor types and has been implicated in the proliferation, migration, and invasion of these tumors (8-11). In the central nervous system, CLIC1 protein expression is elevated upon amyloid β-peptide treatment in neonatal rat microglia. Inhibition of CLIC1 prevents neuronal apoptosis in neurons co-cultured with amyloid β-peptide treated microglia (12). Further studies indicate that CLIC1 translocates from the cytosol to the plasma membrane of microglia upon exposure to amyloid β-peptide, and contributes to the subsequent neurotoxicity through generation of superoxide anions (13). These discoveries implicate CLIC1 as a possible therapeutic target for Alzheimer’s disease.

    For Research Use Only. Not For Use In Diagnostic Procedures.
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