PMID: 6403049Feb 16, 1983Paper

Epidermal growth factor enhances acetylation of nuclear proteins in cultured human liver cells

Biochimica Et Biophysica Acta
Y Kaneko

Abstract

Addition of epidermal growth factor (EGF) to Chang liver cells in a low serum culture causes a long-lasting, two- to three-fold increase in the acetylation of nuclear proteins. This EGF effect is manifested before an increase of cell proliferation in response to EGF. Studies by SDS-polyacrylamide gel electrophoresis and isoelectric focusing show that both histones and acid-insoluble proteins of lower molecular weights are acetylated upon administration of EGF. Tumor promoter teleocidin, which inhibits internalization and nuclear accumulation of EGF, acts antagonistically with EGF in enhancing the acetylation of nuclear proteins. Lysosomal inhibitor chloroquine enhances nuclear accumulation of EGF but has no significant effects on the stimulation of nuclear protein acetylation by EGF. These data appear to suggest that the EGF-enhancement of the acetylation of nuclear proteins is mediated by the steps such as an internalization or nuclear accumulation of EGF or EGF-receptor complex.

References

Jun 1, 1978·Proceedings of the National Academy of Sciences of the United States of America·M Das, C F Fox
Jul 1, 1978·Proceedings of the National Academy of Sciences of the United States of America·H HaiglerS Cohen
Jan 1, 1976·Experientia·S P RoseH Herschman
Jan 26, 1972·Biochimica Et Biophysica Acta·O Vesterberg
Mar 28, 1973·Biochimica Et Biophysica Acta·G de Villiers Graaff, C Von Holt
Jun 1, 1980·Proceedings of the National Academy of Sciences of the United States of America·A C KingP Cuatrecasas
Jul 30, 1981·Biochemical and Biophysical Research Communications·A B SchreiberJ Schlessinger
Mar 1, 1980·Proceedings of the National Academy of Sciences of the United States of America·N SavionD Gospodarowicz

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Citations

Aug 31, 1987·Biochemical and Biophysical Research Communications·J L StaeckerH C Pitot
Aug 30, 1988·Biochemical and Biophysical Research Communications·Y KanekoH Oka

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