EC Number |
General Information |
Reference |
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2.7.11.8 | drug target |
FASTK is an important protein with its valuable implications in various diseases as it serves as a potential drug target |
757248 |
2.7.11.8 | drug target |
inhibitors of Fas-activated serine/threonine kinase may be exploited as potential anticancer agents |
761934 |
2.7.11.8 | drug target |
restoration of FASTK expression through genetic approaches might be a promising therapeutic strategy for alcoholic cardiomyopathy (ACM) |
762364 |
2.7.11.8 | malfunction |
ablating enzyme expression in cultured cells and mice results specifically in loss of ND6 mRNA and reduced complex I activity in vivo |
738004 |
2.7.11.8 | malfunction |
compared to wild type control, alcohol-related myocardial morphological (hypertrophy, fibrosis and cardiomyocyte apoptosis) and functional (reduced ejection fraction and compromised cardiomyocyte contraction) anomalies are worsened in FASTK deficient mice |
762364 |
2.7.11.8 | malfunction |
macrophages from FASTK-/- mice exhibit a marked increase in nonopsonic phagocytosis of bacteria. Activity of mitochondrial respiratory complex I is specifically reduced by almost 50% in FASTK-/- macrophages |
761639 |
2.7.11.8 | physiological function |
the enzyme (FASTK) is a mitochondria-associated nuclear protein that inhibits Fas- and UV-induced apoptosis |
757248 |
2.7.11.8 | physiological function |
the enzyme (FASTK) is implicated in the apoptotic evasion and, hence, the development of cancer |
761934 |
2.7.11.8 | physiological function |
the enzyme is a key post-transcriptional regulator of mitochondrial gene expression. Accelerated FASTK mRNA degradation induced by oxidative stress is responsible for the destroyed myocardial mitochondrial gene expression and respiratory function in alcoholic cardiomyopathy |
762364 |
2.7.11.8 | physiological function |
the mitochondrial isoform is essential for ND6 mRNA biogenesis and complex I activity |
738004 |