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Results 1 - 10 of 21 > >>
EC Number
General Information
Commentary
Reference
malfunction
ATP citrate lyase knockdown induces proliferation arrest, cell-cycle arrest, and apoptosis in cancer cells and results in elevated expression of acyl-CoA synthetase short-chain family member 2
malfunction
deletion of the enzyme results in a complete loss of self and female fertility as well as a reduction in asexual reproduction, virulence, and trichothecene production. Although lipid synthesis is not affected by enzyme deletion, histone acetylation is dramatically reduced in the enzyme deletion mutants during sexual development
malfunction
enzyme activity inhibition as well as gene silencing lead to reduced nitric oxide, reactive oxygen species and prostaglandin E2 inflammatory mediators
malfunction
enzyme inactivation decreases fatty acid synthesis by 60 to 80%
malfunction
enzyme knockdown triggers cellular senescence and activation of tumor suppressor p53
malfunction
inhibition of the enzyme suppresses in vitro glioblastoma cell migration, clonogenicity and brain invasion under glycolytic conditions and enhances the suppressive effects of a Met inhibitor on cell migration
malfunction
loss of ATP-citrate lyase results in severe developmental effects, with the production of asexual spores (conidia) being greatly reduced and a complete absence of sexual development
malfunction
overexpression of the enzyme is observed in nonalcoholic fatty liver disease. Increased enzyme activity is associated with hypocituria, nonalcoholic fatty liver disease, and tumor cell growth. Decreased enzyme activity is associated with type 2 diabetes. ACLY knockdown or inhibition leads to a decrease in glucose-induced insulin secretion
metabolism
DNA methyltransferase 1 is regulated by ATP-citrate lyase
metabolism
involved in lung cancer pathogenesis
Results 1 - 10 of 21 > >>