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).
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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