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논문 기본 정보

자료유형
학술저널
저자정보
변상경 (한국생명공학연구원) 안태현 (한국생명공학연구원) 손민정 (한국생명공학연구원) 이다솜 (한국생명공학연구원) 강현섭 (한국생명공학연구원) 이은우 (한국생명공학연구원) 한백수 (한국생명공학연구원) 김원곤 (한국생명공학연구원) 배광희 (한국생명공학연구원) 오경진 (한국생명공학연구원) 이상철 (한국생명공학연구원)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제40권 제9호
발행연도
2017.9
수록면
667 - 676 (10page)
DOI
10.14348/molcells.2017.0116

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Abnormal differentiation of muscle is closely associated with aging (sarcopenia) and diseases such as cancer and type II diabetes. Thus, understanding the mechanisms that regulate muscle differentiation will be useful in the treatment and prevention of these conditions. Protein lysine acetylation and methylation are major post-translational modification mecha-nisms that regulate key cellular processes. In this study, to elucidate the relationship between myogenic differentiation and protein lysine acetylation/methylation, we performed a PCR array of enzymes related to protein lysine acetylation/methylation during C2C12 myoblast differentiation. Our results indicated that the expression pattern of HDAC11 was substantially increased during myoblast differentiation. Fur-thermore, ectopic expression of HDAC11 completely inhibited myoblast differentiation, concomitant with reduced expression of key myogenic transcription factors. However, the catalytically inactive mutant of HDAC11 (H142/143A) did not impede myoblast differentiation. In addition, wild-type HDAC11, but not the inactive HDAC11 mutant, suppressed MyoD-induced promoter activities of MEF2C and MYOG (Myogenin), and reduced histone acetylation near the E-boxes, the MyoD binding site, of the MEF2C and MYOG promoters. Collectively, our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.

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