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TRAP1 encodes a mitochondrial chaperone protein that is member of the heat shock protein 90 (HSP90) family. Additionally we are shipping TNF Receptor-Associated Protein 1 Antibodies (161) and many more products for this protein.
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TRAP1 is a downstream effector of BRAF (show BRAF Proteins) cytoprotective pathway in mitochondria and TRAP1 targeting may represent a novel strategy to improve the activity of proapoptotic agents in BRAF (show BRAF Proteins)-driven CRC (show CALR Proteins) cells.
the association of rs2679860 polymorphisms of TGFBRAP1 (show TGFBRAP1 Proteins) and DBP (show GC Proteins) variation as well as plasma levels of TGF-beta1 (show TGFB1 Proteins)
Our results indicate that GRP94 (show HSP90B1 Proteins) and TRAP1 might contribute more to the carcinogenesis or biology of SCLC than HSP90alpha (show HSP90AA2 Proteins) and HSP90beta (show HSP90AB1 Proteins)
A previously unobserved coiled-coil dimer conformation may precede dimer closure. TRAP1 exists in an autoinhibited state with the ATP lid bound to the ATP-binding pocket. ATP displaces this and signals the cis (show CISH Proteins)-bound ATP status to the next subunit.
results of the present study show that TRAP1 provides cardioprotection against myocardial I/R by ameliorating mitochondrial dysfunction
a correlation between TRAP1 and AKT expression is found in vivo in human colorectal tumours. These results provide new insights into TRAP1 role in the regulation of cell migration in cancer cells, tumour progression and metastatic mechanisms.
TRAP1 expression was associated with increased risk of lymph node metastasis, while high TRAP1 expression correlated with poor prognosis in esophageal squamous cell cancer.
Our findings demonstrate that SDH inhibition by TRAP1 is oncogenic not only by inducing pseudohypoxia, but also by protecting tumor cells from oxidative stress
crystal structure of the mitochondrial Hsp90, TRAP1, revealed an extension of the N-terminal beta-strand previously shown to cross between protomers in the closed state
Oxidative stress in ulcerative colitis could lead to the increase of cytoprotective protein TRAP1, which in turn could promote cancer progression by preventing or protecting the oxidative damaged epithelial cells from undergoing apoptosis.
Data show that the overexpression of heat shock protein 75 (Hsp75) decreased neural stem cells (NSCs) apoptosis and preserved mitochondrial membrane potential.
TRAP-1-/- mice are viable and show reduced incidence of age-associated pathologies. Loss of TRAP-1 upregulates oxidative phosphorylation and glycolysis transcriptomes.
overexpression of TRAP1 leads to mitochondrial aberrations, including an increase in basal ROS (show ROS1 Proteins) levels and decrease in mitochondrial biogenesis, together with a decrease in peroxisome proliferator-activated receptor gamma (show PPARG Proteins) coactivator-1alpha mRNA levels
Early mesangial nephritis initiates a cascade of inflammatory signals that lead to up-regulation of Trap1 and a consequent down-regulation of renal DNaseI (show DNASE1 Proteins) by transcriptional interference.
TRAP1 regulates a metabolic switch between oxidative phosphorylation and aerobic glycolysis in immortalized mouse fibroblasts.
These data identify TRAP-1 as a novel mitochondrial survival factor differentially expressed in localized and metastatic prostate cancer compared with normal prostate.
This gene encodes a mitochondrial chaperone protein that is member of the heat shock protein 90 (HSP90) family. The encoded protein has ATPase activity and interacts with tumor necrosis factor type I. This protein may function in regulating cellular stress responses. Alternate splicing results in multiple transcript variants.
TNFR-associated protein 1
, heat shock protein 75 kDa, mitochondrial
, tumor necrosis factor type 1 receptor-associated protein
, HSP 75
, tumor necrosis factor type 1 receptor associated protein
, TGF beta receptor associated protein -1
, TGF-beta receptor-associated protein 1
, transforming growth factor-beta receptor-associated protein 1