TRAP1/HSP75 Antibody recognizes endogenous levels of total TRAP1 protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu150 of human TRAP1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
原厂资料:
Specificity / Sensitivity
TRAP1/HSP75 Antibody recognizes endogenous levels of total TRAP1 protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu150 of human TRAP1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
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-linkedPINK1mutations 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)