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导入大鼠L6成肌细胞的人类心脏肌动蛋白基因的调控表明其肌生成程序存在缺陷。

Regulation of a human cardiac actin gene introduced into rat L6 myoblasts suggests a defect in their myogenic program.

作者信息

Hickey R, Skoultchi A, Gunning P, Kedes L

出版信息

Mol Cell Biol. 1986 Sep;6(9):3287-90. doi: 10.1128/mcb.6.9.3287-3290.1986.

Abstract

The rat myogenic cell line L6E9 induces skeletal but not cardiac alpha-actin mRNA upon fusion to form myotubes. However, when a human cardiac alpha-actin gene was introduced into L6E9 myoblasts, differentiation of the cells led to the accumulation of human gene transcripts in parallel with those derived from the endogenous skeletal alpha-actin gene. This result demonstrates that factors which direct rat myogenesis can regulate a muscle gene from another species and that the L6E9 cells may have a defect in their ability to activate endogenous cardiac actin gene expression.

摘要

大鼠成肌细胞系L6E9在融合形成肌管时可诱导骨骼肌而非心肌α-肌动蛋白mRNA的产生。然而,当将人类心脏α-肌动蛋白基因导入L6E9成肌细胞时,细胞分化导致人类基因转录本的积累,且与内源性骨骼肌α-肌动蛋白基因产生的转录本平行。这一结果表明,指导大鼠肌肉生成的因子可以调节来自另一个物种的肌肉基因,并且L6E9细胞在激活内源性心脏肌动蛋白基因表达的能力上可能存在缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46b3/367068/253fe42338ab/molcellb00093-0274-a.jpg

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