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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 (189) and TNF Receptor-Associated Protein 1 Proteins (9) and many more products for this protein.
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TRAP1 inhibition may be regarded as potential strategy to target specific features of human thyroid cancers, i.e., cell proliferation and resistance to apoptosis.
TRAP1 regulates stemness and Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) pathway in colorectal cancer.
data show that TRAP1 acts downstream of PINK1 and HTRA2 for mitochondrial fine tuning, whereas TRAP1 loss of function leads to reduced control of energy metabolism, ultimately impacting mitochondrial membrane potential.
This review summarizes how metabolism, chemoresistance, inflammation, and epithelial-to-mesenchymal transition are strictly interconnected, and how TRAP1 stays at the crossroads of these processes, thus shedding new lights on molecular networks at the basis of ovarian cancer. [review]
These data suggest that TRAP1 protein network may provide a prognostic signature in human metastatic colorectal carcinomas
TRAP1 is relevant in the control of key cell cycle regulators in tumor cells. TRAP1/TBP7 (show PSMC4 ELISA Kits) quality control of CDK1 (show CDK1 ELISA Kits) and MAD2 (show MAD2L1 ELISA Kits) contributes mechanistically to the regulation of mitotic entry and transit.
TRAP1 is often deleted in high-grade serous ovarian cancer patients.
TRAP1 increases cell proliferation, reduces apoptosis, and promotes cell invasion without changes in mitochondrial bioenergetics. Therefore, TRAP1 is a driver of prostate cancer in vivo and an "actionable" therapeutic target.
overexpression of TRAP1 might contribute to tumor cell local invasion of colorectal cancer
Increased TRAP1 expression was significantly associated with EOC stages.
show that TRAP1 could protect the mitochondrial structure in renal tubular epithelial cells; maintain the levels of mitochondrial membrane potential, ATP, and mitochondrial DNA copy number
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 ELISA Kits) levels and decrease in mitochondrial biogenesis, together with a decrease in peroxisome proliferator-activated receptor gamma (show PPARG ELISA Kits) 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 ELISA Kits) 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.
The crystal structure of full-length TRAP1, the mitochondrial Hsp90 (show HSP90 ELISA Kits) molecular chaperone (show HSP90AA1 ELISA Kits), in a catalytically active closed state is presented.
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