Render Target: SSR
Render Timestamp: 2024-11-14T23:07:53.819Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:57:02.028
Product last modified at: 2024-10-23T21:15:11.603Z
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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.

TRAP1/HSP75 (D3D7N) Rabbit mAb #92345

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 75
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunofluorescence (Immunocytochemistry) 1:100

    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

    TRAP1/HSP75 (D3D7N) Rabbit mAb recognizes endogenous levels of total TRAP1/HSP75 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro70 of human TRAP1/HSP75 protein.

    Background

    TNF receptor-associated protein 1 (TRAP1), also known as HSP75, is a mitochondrial chaperone and ATPase that was originally identified as a protein that interacts with the TNF receptor. Although a member of the HSP90 family, TRAP1 is not heat-inducible but is upregulated by glucose deprivation, oxidative injury, and UV irradiation. An amino-terminal mitochondrial localization sequence results in localization of TRAP1 within mitochondria (1). Overexpression of TRAP1 decreases oxidative stress, suggesting a protective role in ischemia injury (2). Research studies demonstrate that silencing of TRAP1 enhances cytochrome C release and apoptosis, with additional evidence indicating that TRAP1 can protect cells from cell death by inhibiting the generation of reactive oxygen species (3). TRAP1 is a substrate of the mitochondrial serine/threonine kinase PINK1, whose corresponding gene is mutated in some forms of early-onset Parkinson's disease (PD). PINK1 protects cells from oxidative stress-induced cell death by suppressing release of cytochrome C from mitochondria. PD-linked PINK1 mutations impair the ability of PINK1 to phosphorylate TRAP1 and leads to impaired cell survival (4). Finally, TRAP1 alleviates α-synuclein induced toxicity and rescues the PINK1 loss-of-function phenotype (5).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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