Abstract
Tyrosine aminotransferase induction has been studied in hepatocytes from untreated, partially and fully glucocorticoid-induced rats: enzyme activities were initially 12.9 +/- 1.7 (n = 16), 41.4 +/- 3.2 (n = 6) and 117.9 +/- 10.5 (n = 7) munits/mg protein, respectively. Untreated or fully induced hepatocytes maintain initial levels, whereas partially induced hepatocytes increase their tyrosine aminotransferase activity even in the presence of actinomycin D. Fully induced hepatocytes possess a normal protein synthetizing machinery and the mechanisms to degrade selectively tyrosine aminotransferase. The effect of progesterone treatment is consistent with these cells retaining a high dexamethasone level. Glucagon induces tyrosine aminotransferase via its second messenger, cyclic AMP. This induction decreases dramatically with in vivo glucocorticoid treatment. Time courses and effects of inhibitors are consistent with these in vivo and in vitro treatments being alternative methods of inducing tyrosine aminotransferase by the same basic pretranslational step.
TY - JOUR
T1 - The regulation of hepatic tyrosine aminotransferase.
A1 - Evans,P J,
PY - 1981/11/5/pubmed
PY - 1981/11/5/medline
PY - 1981/11/5/entrez
SP - 433
EP - 44
JF - Biochimica et biophysica acta
JO - Biochim Biophys Acta
VL - 677
IS - 3-4
N2 - Tyrosine aminotransferase induction has been studied in hepatocytes from untreated, partially and fully glucocorticoid-induced rats: enzyme activities were initially 12.9 +/- 1.7 (n = 16), 41.4 +/- 3.2 (n = 6) and 117.9 +/- 10.5 (n = 7) munits/mg protein, respectively. Untreated or fully induced hepatocytes maintain initial levels, whereas partially induced hepatocytes increase their tyrosine aminotransferase activity even in the presence of actinomycin D. Fully induced hepatocytes possess a normal protein synthetizing machinery and the mechanisms to degrade selectively tyrosine aminotransferase. The effect of progesterone treatment is consistent with these cells retaining a high dexamethasone level. Glucagon induces tyrosine aminotransferase via its second messenger, cyclic AMP. This induction decreases dramatically with in vivo glucocorticoid treatment. Time courses and effects of inhibitors are consistent with these in vivo and in vitro treatments being alternative methods of inducing tyrosine aminotransferase by the same basic pretranslational step.
SN - 0006-3002
UR - https://www.unboundmedicine.com/medline/citation/6117330/The_regulation_of_hepatic_tyrosine_aminotransferase_
L2 - https://linkinghub.elsevier.com/retrieve/pii/0304-4165(81)90257-9
DB - PRIME
DP - Unbound Medicine
ER -