Abstract
TRIM72 is known to be involved in the negative feedback regulation of myogenesis by targeting insulin receptor substrate-1. Here, we found that TRIM72 was more highly expressed in oxidative muscle with the higher activity of MEF2, compared to glycolytic muscle. Indeed, TRIM72 promoter contained an evolutionarily conserved MEF2 site juxtaposed to E-box. TRIM72 promoter activity was decreased by the site-directed mutagenesis of either E-boxes or a MEF2 site and synergistically enhanced by MyoD (or myogenin) and MEF2, which were associated with proximal E-box, and MEF2 site of the TRIM72 promoter, respectively. Taken together all these data, we concluded that the synergism of MyoD (or myogenin) and MEF2 is necessary for TRIM72 expression during C2C12 differentiation.
Original language | English |
---|---|
Pages (from-to) | 238-245 |
Number of pages | 8 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 396 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2010 May 28 |
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Keywords
- C2C12
- MEF2
- MyoD
- Myogenin
- TRIM72
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Molecular Biology
Cite this
TRIM72, a novel negative feedback regulator of myogenesis, is transcriptionally activated by the synergism of MyoD (or myogenin) and MEF2. / Jung, Soon Young; Ko, Young-Gyu.
In: Biochemical and Biophysical Research Communications, Vol. 396, No. 2, 28.05.2010, p. 238-245.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - TRIM72, a novel negative feedback regulator of myogenesis, is transcriptionally activated by the synergism of MyoD (or myogenin) and MEF2
AU - Jung, Soon Young
AU - Ko, Young-Gyu
PY - 2010/5/28
Y1 - 2010/5/28
N2 - TRIM72 is known to be involved in the negative feedback regulation of myogenesis by targeting insulin receptor substrate-1. Here, we found that TRIM72 was more highly expressed in oxidative muscle with the higher activity of MEF2, compared to glycolytic muscle. Indeed, TRIM72 promoter contained an evolutionarily conserved MEF2 site juxtaposed to E-box. TRIM72 promoter activity was decreased by the site-directed mutagenesis of either E-boxes or a MEF2 site and synergistically enhanced by MyoD (or myogenin) and MEF2, which were associated with proximal E-box, and MEF2 site of the TRIM72 promoter, respectively. Taken together all these data, we concluded that the synergism of MyoD (or myogenin) and MEF2 is necessary for TRIM72 expression during C2C12 differentiation.
AB - TRIM72 is known to be involved in the negative feedback regulation of myogenesis by targeting insulin receptor substrate-1. Here, we found that TRIM72 was more highly expressed in oxidative muscle with the higher activity of MEF2, compared to glycolytic muscle. Indeed, TRIM72 promoter contained an evolutionarily conserved MEF2 site juxtaposed to E-box. TRIM72 promoter activity was decreased by the site-directed mutagenesis of either E-boxes or a MEF2 site and synergistically enhanced by MyoD (or myogenin) and MEF2, which were associated with proximal E-box, and MEF2 site of the TRIM72 promoter, respectively. Taken together all these data, we concluded that the synergism of MyoD (or myogenin) and MEF2 is necessary for TRIM72 expression during C2C12 differentiation.
KW - C2C12
KW - MEF2
KW - MyoD
KW - Myogenin
KW - TRIM72
UR - http://www.scopus.com/inward/record.url?scp=77952741352&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77952741352&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2010.04.072
DO - 10.1016/j.bbrc.2010.04.072
M3 - Article
C2 - 20399744
AN - SCOPUS:77952741352
VL - 396
SP - 238
EP - 245
JO - The BMJ
JF - The BMJ
SN - 0730-6512
IS - 2
ER -