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Retinoic acid‐induced changes in differentiation‐defective embryonal carcinoma RAC65 cells
Author(s) -
Malý Petr,
Dráber Petr
Publication year - 1992
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(92)81377-x
Subject(s) - retinoic acid , embryonal carcinoma , chemistry , microbiology and biotechnology , carcinoma , cellular differentiation , medicine , biology , biochemistry , gene
RAC65 is a mutant clone of mouse embryonal carcinoma cells, P19, which does not undergo terminal differentiation upon treatment with retinoic acid (RA), RAC65 cells express a truncated RA receptor α (RARα) which, however, does not fully explain their defect. Here we show that RAC65 cells exhibit an additional defect in RARα mRNA which may reflect a defect in RNA splicing. The parental and mutant cells also differ in their capacities to bind [ 3 H]RA into nuclear fractions and in expression of cellular RA binding protein (CRABP) mRNA after treatment with RA. The combined data suggest that the deffect in RAC65 RARα results in reduced expression of the CRABP gene after RA treatment and, therefore, increased flow of RA into the nucleus.