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Results find that head and neck squamous cell carcinoma (HNSCC) tumor tissues and cell lines had high levels of CTMP expression. These data suggest that CTMP functions as a positive regulator of Akt and facilitates HNSCC invasion such as LN metastasis by regulating EMT in a Snail-dependent manner indicating the oncogenic activity of CTMP in HNSCC, and its expression is an independent predictor of clinical prognosis.
CTMP expression may be considered as a prognostic biomarker in HER2-enriched breast cancer and high expression may indicate a utility for AKT-inhibition in these patients.
Suggest that CTMP may therefore play a critical role in mitochondrial-mediated apoptosis in lung cancer cells.
Data show low or moderate methylation was found in seven selected genes BAD, BBC3, CAV1, CDK2AP1, NPM1, PRKCDBP and THEM4.
CTMP induces translocation of Akt to the membrane and thereby increases the level of Akt phosphorylation. As a result, CTMP enhances various cellular activities that are principally mediated by the PI3-kinase/Akt pathway.
Proper maturation of CTMP is essential for its pro-apoptotic function. CTMP delays PKB phosphorylation following cell death induction, suggesting that CTMP regulates apoptosis via inhibition of PKB.
Phosphorylation on Ser37/Ser38 of CTMP is important for the prevention of mitochondrial localization of CTMP, eventually leading to cell death by binding to heat shock protein 70.
Results suggest that Akt is phosphorylated and translocated to nucleus after traumatic brain injury (TBI) to exert neuroprotective effects; however, CTMP is simultaneously triggered to inhibit the phosphorylation of Akt
Protein kinase B (PKB) is a major downstream target of receptor tyrosine kinases that signal via phosphatidylinositol 3-kinase. Upon cell stimulation, PKB is translocated to the plasma membrane, where it is phosphorylated in the C-terminal regulatory domain. The protein encoded by this gene negatively regulates PKB activity by inhibiting phosphorylation. Transcription of this gene is commonly downregulated in glioblastomas.
thioesterase superfamily member 4
, acyl-coenzyme A thioesterase THEM4
, C-terminal modulator protein
, acyl-CoA thioesterase THEM4
, carboxyl-terminal modulator protein