蛋白激酶A（PKA）调控经二丁酰环磷腺苷（db-cAMP）处理的小鼠L5178Y淋巴瘤细胞中拓扑异构酶I mRNA的水平。
PKA controls a level of topoisomerase I mRNA in mouse L5178Y lymphoma cells treated with db-cAMP.
作者信息
Czerwinski R M, Nieznanski K, Sochanowicz B, Staron K
机构信息
Institute of Biochemistry, Warsaw University, Poland.
出版信息
Mol Biol Rep. 1994 Mar;19(2):93-7. doi: 10.1007/BF00997153.
The level of topoisomerase I mRNA was measured in cells of two mouse lymphoma (LY) sublines treated with db-cAMP. A transient increase of the level was observed to be of about 60% of the basic level and to have maximum after the 3 h treatment of LY-S cells. The increase in LY-R subline was two-fold lower. The activity of PKA in a cytosol fraction of LY-S cells was 1.75 times higher than that in LY-R cells. The activity of PKA in membranes and nuclear fraction did not differ significantly in both cell types. When the activity of PKA in LY-S cells was inhibited with H8, no increase of the level of topoisomerase I mRNA was observed upon db-cAMP treatment of cells. We suggest that the activity of PKA in the cytosol controls the expression of topoisomerase I gene in LY cells at high concentration of cAMP.
用双丁酰环磷腺苷（db - cAMP）处理两个小鼠淋巴瘤（LY）亚系的细胞后，测定了拓扑异构酶I mRNA的水平。观察到该水平短暂升高，约为基础水平的60%，且在LY - S细胞处理3小时后达到最大值。LY - R亚系的升高幅度低两倍。LY - S细胞胞质溶胶部分的蛋白激酶A（PKA）活性比LY - R细胞高1.75倍。两种细胞类型中，膜和核部分的PKA活性无显著差异。当用H8抑制LY - S细胞中的PKA活性时，用db - cAMP处理细胞后未观察到拓扑异构酶I mRNA水平的升高。我们认为，在高浓度环磷腺苷（cAMP）时，胞质溶胶中的PKA活性控制着LY细胞中拓扑异构酶I基因的表达。
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