在終極肌肉分化時，肌肉性bHLH轉錄因子對PGC-1α的調控; Myogenic basic helix-loop-helix transcription factors regulate PGC-1α during terminal myogenic differentiation

NCUIR > college of Health Sciences and Technology > Graduate Institute of Life Science > Electronic Thesis & Dissertation > Item 987654321/6390

Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/6390

Title:	在終極肌肉分化時，肌肉性bHLH轉錄因子對PGC-1α的調控;Myogenic basic helix-loop-helix transcription factors regulate PGC-1α during terminal myogenic differentiation
Authors:	黃凱民;Kai-min Huang
Contributors:	生命科學研究所
Keywords:	過氧化物酶增殖體激活受體γ共激活蛋白1;慢速收縮肌;Stra13;PGC-1α;P/CAF;MyoD;slow-twitch muscle fiber
Date:	2007-07-10
Issue Date:	2009-09-22 10:18:44 (UTC+8)
Publisher:	國立中央大學圖書館
Abstract:	成熟肌肉細胞一般分為兩種型態，第一型慢速收縮肌跟第二型快速收縮肌。在慢速收縮肌中，我們發現含有大量粒線體，因此可以藉由氧化電子傳遞鏈提供大量ATP提供人體生存所需的能量，反觀，快速收縮肌在能量代謝方面比較偏向醣解代謝，在外觀上，因為慢速收縮肌含有多血紅蛋白所以比較偏向紅色。目前我們知道PPAR-γ輔助轉錄因子PGC-1α在肌肉纖維的決定上有莫大關鍵性，而成體上主要表現在慢速收縮肌中。而之前文獻指出，轉殖鼠系統中，若過量表現PGC-1α在肌肉細胞中，會使得肌肉細胞走向慢速肌肉的趨勢，從之前觀察，我們知道在PGC-1α啟動子區有兩個非常保留E-box(CANNTG)，較轉錄起始點遠的E-box我們稱為E1-box，較轉錄起始點近的E-box稱為E2-box，由之前觀察我們知道MyoD 活化PGC-1α時，是藉由直接結合於PGC-1α啟動區的E2-box。藉由生物資訊分析另一個E-box是可能被Stra13所結合。從promoter assay，我們知道Stra13會抑制MyoD所主導PGC-1α的活化，而可能藉由的方式是經由跟MyoD競爭coactivator-P/CAF，而導致MyoD活化PGC-1α有所被抑制。 Skeletal muscle are generally classified as two types – type I (slow - twitch) and type II (fast - twitch). The former is rich in mitchondria and thus provides constant ATP through oxidative metabolism. The latter depends on the glycolytic metabolism as the energy source. PGC-1α is a transcriptional coactivator mainly expressed in the slow-twitch fibers. Previous studies indicated that over-expression of PGC-1α promotes the conversion from fast-twitch fibers to slow-twitch fibers. According to previous observations, we know that the E2-box on the PGC-1α promoter is essential for MyoD-mediated transactivation. In this study, we found that Stra13, a putative E1-box binding transcriptional repressor, repressed the MyoD mediated PGC-1α promoter activation. The interaction between MyoD and Stra13 was almost undetectable by GST-Pull down assay and EMSA. In addition, over-expression of P/CAF, but not CBP, can rescue the Stra13-mediated repression. These data suggest that Stra13 represses MyoD-mediated PGC-1 activation by sequestering P/CAF from MyoD.
Appears in Collections:	[Graduate Institute of Life Science] Electronic Thesis & Dissertation

Files in This Item:

File	Size	Format

社群 sharing

Loading...