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	
2.7.11.8	physiological function	the mitochondrial isoform of FASTK modulates nonopsonic phagocytosis of bacteria by macrophages via regulation of respiratory complex I	761639