GATA elements control repression of cardiac troponin I promoter activity in skeletal muscle cells.
GATA elements control repression of cardiac troponin I promoter activity in skeletal muscle cells.
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DOI：
10.1186/1471-2199-8-78
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发表时间：
2007-09-17
影响因子：
--
通讯作者：
Schiaffino S
中科院分区：
文献类型：
--
作者：
Di Lisi R;Picard A;Ausoni S;Schiaffino S
我们先前报道了心肌肌钙蛋白I（cTnI）启动子驱动心肌细胞和转基因小鼠中报告基因的心脏特异性表达，并且加塔元件的破坏使培养的心肌细胞中cTnI启动子失活。我们现在已经研究了cTnI启动子加塔元件在骨骼肌细胞中的作用。加塔元件的突变或缺失诱导再生骨骼肌和培养骨骼肌细胞中cTnI启动子的强烈转录激活。电泳迁移率变动分析表明，C2 C12肌细胞核提取物中存在的蛋白质结合cTnI启动子中存在的加塔基序。然而，加塔蛋白复合物的形成既不被特异于加塔-2、-3和-4（肌细胞中存在的仅有的加塔转录物）的抗体减少也不被超移位。这些发现表明，cTnI基因启动子在骨骼肌细胞中被GATA样因子抑制，并为进一步研究这些因子开辟了道路。
We reported previously that the cardiac troponin I (cTnI) promoter drives cardiac-specific expression of reporter genes in cardiac muscle cells and in transgenic mice, and that disruption of GATA elements inactivates the cTnI promoter in cultured cardiomyocytes. We have now examined the role of cTnI promoter GATA elements in skeletal muscle cells. Mutation or deletion of GATA elements induces a strong transcriptional activation of the cTnI promoter in regenerating skeletal muscle and in cultured skeletal muscle cells. Electrophoretic mobility shift assays show that proteins present in nuclear extracts of C2C12 muscle cells bind the GATA motifs present in the cTnI promoter. However, GATA protein complex formation is neither reduced nor supershifted by antibodies specific for GATA-2, -3 and -4, the only GATA transcripts present in muscle cells. These findings indicate that the cTnI gene promoter is repressed in skeletal muscle cells by GATA-like factors and open the way to further studies aimed at identifying these factors.
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影响因子：
4.2
作者：
VITADELLO, M;SCHIAFFINO, MV;SCHIAFFINO, S
通讯作者：
SCHIAFFINO, S
影响因子：
2.7
作者：
Li, Shanru;Lu, Min Min;Morrisey, Edward E.
通讯作者：
Morrisey, Edward E.
DOI：
10.1073/pnas.0308035101
发表时间：
2004-07-20
影响因子：
11.1
作者：
McCullagh, KJA;Calabria, E;Schiaffino, S
通讯作者：
Schiaffino, S
影响因子：
4.8
作者：
Dhar, M;Mascareno, EM;Siddiqui, MAQ
通讯作者：
Siddiqui, MAQ
影响因子：
2.7
作者：
Iwahori, A;Fraidenraich, D;Basilico, C
通讯作者：
Basilico, C