Gene interactions and pathways from curated databases and text-mining

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CRAT — INS

Text-mined interactions from Literome

Hernandez et al., FEBS Lett 2001 : Indeed, co-transfection of brown adipocytes with DeltaAkt precluded the transactivation of GLUT4-CAT promoter by insulin in a similar fashion as a dominant negative form of PI3-kinase
Spandidos et al., Anticancer Res 1990 : It was found that, at optimal concentrations, insulin , epidermal growth factor and hydrocortisone regulate positively the expression of CAT from the HIV LTR in rat RFBHIV1-1 but not in human SVTGHIV1-1 cells
Jacob et al., Mol Cell Endocrinol 1995 (Pituitary Neoplasms...) : Insulin and cAMP stimulate prolactin gene transcription and prolactin-CAT expression in rat pituitary tumor GH cells
Hu et al., Endocrinology 1996 : Insulin at 10 ( -7 ) M resulted in a 42.1 +/- 9.8 % suppression of CAT activity in hepatocytes from pituitary-intact animals transfected with a CAT reporter plasmid containing 1671 bp of the 5'-flanking region of the rat IGFBP-1 gene
Gaben et al., Oncogene 1996 : A dominant negative ras mutant ( Ha-Ras Asn-17 ) cancelled both the basal and insulin induced CAT expression in the BP-A31 but not in the Ras2 cells
Streeper et al., J Biol Chem 1997 : To identify the insulin response sequence (IRS) in the G6Pase promoter through which insulin mediates its action, we have analyzed the effect of insulin on the basal expression of mouse G6Pase-chloramphenicol acetyltransferase (CAT) fusion genes transiently expressed in hepatoma cells ... The presence of this multicomponent IRS may explain why insulin potently inhibits basal G6Pase-CAT expression
Davidović et al., Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 1997 : INS , independent of the dose applied, did not affect CAT activity in control rats, whereas only low INS dose increased the activity of this enzyme in 6-HDA treated rats
Teruel et al., J Cell Physiol 1998 : Transient transfection of dominant negative form of phosphatidylinositol (PI) 3-kinase completely blocked the transactivation of the fusion gene UCP1-CAT induced by either IGF-I or insulin , although inhibition of p70S6kinase with rapamycin does not preclude transactivation of the UCP1 promoter by insulin
Streeper et al., Mol Endocrinol 1998 (Liver Neoplasms, Experimental) : Deletion of the PEPCK-like IRS motif had no effect on the stimulation of CAT expression by insulin
Valverde et al., Biochem J 1999 : Inhibition of phosphoinositide (PI) 3-kinase activity with chemical agents such as wortmannin or LY294002 partially blocked insulin induced GLUT4 mRNA accumulation, insulin induced GLUT4 protein content, GLUT4-CAT transactivation and glucose uptake