Glucocorticoid induction of CRE-binding protein isoform mRNAs in rat C6 glioma cells

• Published in: Nucleic acids research Vol. 20; no. 4; pp. 825 - 829
• Main Authors: Jungmann, Richard A., Wang, Xue-song, Milkowski, Deborah M., Short, Marc L.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 25-02-1992
• Subjects: Animals; Base Sequence; Biological and medical sciences; Blotting, Northern; Blotting, Western; Cell Line; Cyclic AMP Response Element-Binding Protein; Dexamethasone - pharmacology; DNA-Binding Proteins - genetics; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - drug effects; Molecular and cellular biology; Molecular genetics; Molecular Sequence Data; Rats; RNA, Messenger - genetics; Transcription Factors - genetics; Transcription. Transcription factor. Splicing. Rna processing; Molecular form; Rat; Induction; Rodentia; Gene expression; Glucocorticoid; Response element; Binding protein; Vertebrata; Mammalia; Cell line; Messenger RNA; Glioma; Transcription factor
• ISSN: 0305-1048; 1362-4962
• DOI: 10.1093/nar/20.4.825

Mammalian cells express several distinct isoforms of transcription factor CREB (cAMP-responsive element binding protein). At least two forms, α- and ΔCREB, arise through alternative splicing of the CREB gene transcript. In this communication we demonstrate that the mRNAs of several CREB isoforms are expressed in rat C6 glioma cells and that the Intracellular levels of these mRNAs are markedly induced by the synthetic glucocorticoid dexamethasone. Nuclear run-off assays show that the induction occurs, at least in part, through a transcriptlonal mechanism. The enhanced cellular levels of CREB mRNAs are accompanied by increased CREB protein and CRE-binding activity of nuclear extracts as evaluated by immunoblot and Southwestern blot assays.