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EGF — TAT

Text-mined interactions from Literome

Kido et al., FEBS Lett 1987 : Epidermal growth factor (EGF) dose-dependently enhanced the induction of tyrosine aminotransferase and tryptophan oxygenase by glucocorticoids in primary cultures of adult rat hepatocytes without itself having any effect on these enzymes in the absence of glucocorticoids ... EGF had no effect on induction of tyrosine aminotransferase by glucagon or Bt2cAMP
Katunuma et al., Adv Enzyme Regul 1987 (Neoplasms, Experimental) : The induction of tyrosine aminotransferase by glucocorticoid and its amplification by EGF were both inhibited by 1- ( 5-iso-quinoline-sulfonyl ) -2-methylpiperazine, an inhibitor of protein kinase C, and not by N- [ 2- ( methylamino ) -ethyl ] -5-isoquinoline-sulfonamide, an inhibitor of cyclic nucleotide dependent protein kinases, suggesting that the induction and the amplification are mediated by protein kinase C
Auberger et al., Biochem J 1983 : Induction of tyrosine aminotransferase by glucagon or dexamethasone, which, like stimulation of transport, represents a late hormonal effect, was not affected by EGF , PDGF or FCS, but was inhibited by thrombin
Nakamura et al., J Biol Chem 1984 : The membrane-free modulator showed activities for inhibition of DNA synthesis stimulated by insulin with epidermal growth factor and stimulation of tyrosine aminotransferase induction by dexamethasone
Fillat et al., FEBS Lett 1993 (Liver Neoplasms, Experimental) : Epidermal growth factor (EGF) decreased the basal, and blocked the dibutyryl cyclic AMP ( Bt2cAMP ) -induced, expression of P-enolpyruvate carboxykinase ( GTP ) ( PEPCK ) and tyrosine aminotransferase (TAT) genes in both rat hepatocytes in primary culture and the FTO-2B hepatoma cell line