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Induction of Tyrosine Aminotransferase by Dexamethasone, Insulin, and Serum
Dexamethasone induces the synthesis of tyrosine aminotransferase in hepatoma tissue culture (HTC) cells, an established line of rat hepatoma cells in tissue culture. The addition of insulin or dialyzed serum to cells previously induced with dexamethasone in a serum-free medium causes a further doubl...
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Published in: | The Journal of biological chemistry 1972-10, Vol.247 (19), p.6197-6203 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Dexamethasone induces the synthesis of tyrosine aminotransferase in hepatoma tissue culture (HTC) cells, an established line of rat hepatoma cells in tissue culture. The addition of insulin or dialyzed serum to cells previously induced with dexamethasone in a serum-free medium causes a further doubling in tyrosine aminotransferase activity, which is not dependent on concomitant RNA synthesis. The simultaneous addition of maximally effective concentrations of both insulin and serum causes an additive stimulation of tyrosine aminotransferase activity. This result suggests that insulin and serum might either affect different aspects of the control of a single enzyme, or alternatively the synthesis of different isozymes of tyrosine aminotransferase.
Crude extracts of HTC cells induced with dexamethasone alone, dexamethasone plus insulin, or dexamethasone plus serum have been analyzed by titration with antibody to purified rat liver tyrosine aminotransferase, by heat stability, and by electrophoresis on polyacrylamide gels. These methods readily distinguish tyrosine aminotransferase of HTC cell origin from that of renal cell origin. By all three of the techniques used in this study, the tyrosine aminotransferase induced by dexamethasone, insulin, and serum appears to be identical. Thus these three humoral factors all appear to enhance the synthesis of the same enzyme, possibly by affecting different aspects of its post-transcriptional control. |
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ISSN: | 0021-9258 1083-351X |
DOI: | 10.1016/S0021-9258(19)44782-0 |