Myocyte enhancer factor (MEF) 2C

A tissue-restricted member of the MEF-2 family of transcription factors

James F. Martin, John J. Schwarz, Eric N. Olson

Research output: Contribution to journalArticle

209 Citations (Scopus)

Abstract

MEF-2 is a muscle-specific DNA binding activity that recognizes an A+T-rich sequence found in the control regions of numerous muscle-specific genes. The recent cloning of MEF-2 showed that it belongs to the MADS (MCM1, Agamous, Deficiens, and serum-response factor) box family of transcription factors and that MEF-2 mRNA is expressed ubiquitously. Here we describe the cloning of a member of the MEF-2 gene family, referred to as MEF-2C, that is nearly identical to other MEF-2 gene products in the MADS box but diverges from other members of the family outside of this domain. MEF-2C binds the MEF-2 site with high affinity and can activate transcription of a reporter gene linked to tandem copies of that site. In contrast to previously described members of the MEF-2 family, MEF-2C transcripts are highly enriched in skeletal muscle, spleen, and brain of adult mice and are upregulated during myoblast differentiation. These results suggest that the MEF-2 site is a target for a diverse family of proteins that regulates transcription in a variety of cell types.

Original languageEnglish (US)
Pages (from-to)5282-5286
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume90
Issue number11
StatePublished - Jun 1 1993

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MEF2 Transcription Factors
Transcription Factors
Serum Response Factor
Organism Cloning
Genes
Muscles
Myoblasts
Reporter Genes

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

Myocyte enhancer factor (MEF) 2C : A tissue-restricted member of the MEF-2 family of transcription factors. / Martin, James F.; Schwarz, John J.; Olson, Eric N.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 90, No. 11, 01.06.1993, p. 5282-5286.

Research output: Contribution to journalArticle

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