|  Help  |  About  |  Contact Us

Publication : MEF2B is a potent transactivator expressed in early myogenic lineages.

First Author  Molkentin JD Year  1996
Journal  Mol Cell Biol Volume  16
Issue  7 Pages  3814-24
PubMed ID  8668199 Mgi Jnum  J:33568
Mgi Id  MGI:81047 Doi  10.1128/mcb.16.7.3814
Citation  Molkentin JD, et al. (1996) MEF2B is a potent transactivator expressed in early myogenic lineages. Mol Cell Biol 16(7):3814-24
abstractText  There are four members of the myocyte enhancer binding factor 2 (MEF2) family of transcription factors, MEF2A, - B, -C, and -D, that have homology within an amino-terminal MADS box and an adjacent MEF2 domain that together mediate dimerization and DNA binding. MEF2A, -C, and -D have previously been shown to bind an A/T-rich DNA sequence in the control regions of numerous muscle-specific genes, whereas MEF2B was reported to be unable to bind this sequence unless the carboxyl terminus was deleted. To further define the functions of MEF2B, we analyzed its DNA binding and transcriptional activities. In contrast to previous studies, our results show that MEF2B binds the same DNA sequence as other members of the MEF2 family and acts as a strong transactivator through that sequence. Transcriptional activation by MEF2B is dependent on the carboxyl terminus, which contains two conserved sequence motifs found in all vertebrate MEF2 factors. During mouse embryogenesis, MEF2B transcripts are expressed in the developing cardiac and skeletal muscle lineages in a temporospatial pattern distinct from but overlapping with those of the other Mef2 genes. The mouse Mef2b gene maps to chromosome 8 and is unlinked to other Mef2 genes; its intron-exon organization is similar to that of the other vertebrate Mef2 genes and the single Drosophila Mef2 gene, consistent with the notion that these different Mef2 genes evolved from a common ancestral gene.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

15 Bio Entities

Trail: Publication

21 Expression

Trail: Publication