RETINOIC ACID INDUCES LIVER BONE KIDNEY-TYPE ALKALINE-PHOSPHATASE GENE-EXPRESSION IN F9 TERATOCARCINOMA CELLS

RETINOIC ACID INDUCES LIVER BONE KIDNEY-TYPE ALKALINE-PHOSPHATASE GENE-EXPRESSION IN F9 TERATOCARCINOMA CELLS
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DOI:
10.1042/bj2740673
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发表时间:
1991-03-15
影响因子:
4.1
通讯作者:
GARATTINI, E
GARATTINI, E
中科院分区:
生物学3区
文献类型:
--
作者:
GIANNI, M;STUDER, M;GARATTINI, E

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全反式视黄酸(RA)诱导小鼠F9畸胎瘤细胞碱性磷酸酶(ALP)活性的3-8倍,平行于他们向原始内胚层分化。 ALP活性的升高与肝/骨/肾型ALP蛋白和相应转录物的量的增加相关。 RA的这些作用是由于ALP基因转录的激活,而不是mRNA半衰期的增加。 ALP mRNA的诱导不需要从头蛋白质合成,因为它不会被放线菌酮阻断。 二丁酰环AMP,这是已知的诱导F9细胞从原始的壁内胚层的进一步分化,阻止诱导的ALP mRNA的RA。
All-trans retinoic acid (RA) induces alkaline phosphatase (ALP) activity by 3-8-fold in murine F9 teratocarcinoma cells, in parallel with their differentiation towards primitive endoderm. The elevation of ALP activity is associated with increases in the amounts of liver/bone/kidney-type ALP protein and the respective transcript. These effects of RA are due to activation of ALP gene transcription rather than to an increase in the half-life of the mRNA. Induction of ALP mRNA does not require de novo protein synthesis, since it is not blocked by treatment with cycloheximide. Dibutyryl cyclic AMP, which is known to induce further differentiation of F9 cells from the primitive to the parietal endoderm, blocks the induction of ALP mRNA by RA.