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本文引用的文献

1
MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice.微小RNA-208a是小鼠心脏肥大和传导的调节因子。
J Clin Invest. 2009 Sep;119(9):2772-86. doi: 10.1172/JCI36154. Epub 2009 Aug 10.
2
Evidence of MyomiR network regulation of beta-myosin heavy chain gene expression during skeletal muscle atrophy.肌微小 RNA 网络对骨骼肌萎缩过程中β-肌球蛋白重链基因表达的调控作用。
Physiol Genomics. 2009 Nov 6;39(3):219-26. doi: 10.1152/physiolgenomics.00042.2009. Epub 2009 Aug 18.
3
Intrinsic expression of host genes and intronic miRNAs in prostate carcinoma cells.宿主基因和内含子miRNA在前列腺癌细胞中的内在表达。
Cancer Cell Int. 2009 Aug 12;9:21. doi: 10.1186/1475-2867-9-21.
4
MicroRNA-145 regulates OCT4, SOX2, and KLF4 and represses pluripotency in human embryonic stem cells.微小RNA-145调节OCT4、SOX2和KLF4,并抑制人类胚胎干细胞的多能性。
Cell. 2009 May 15;137(4):647-58. doi: 10.1016/j.cell.2009.02.038. Epub 2009 Apr 30.
5
A feedback regulatory loop involving microRNA-9 and nuclear receptor TLX in neural stem cell fate determination.一个涉及微小RNA-9和核受体TLX的反馈调节环路在神经干细胞命运决定中的作用
Nat Struct Mol Biol. 2009 Apr;16(4):365-71. doi: 10.1038/nsmb.1576. Epub 2009 Mar 29.
6
A systematic analysis of intronic sequences downstream of 5' splice sites reveals a widespread role for U-rich motifs and TIA1/TIAL1 proteins in alternative splicing regulation.对5'剪接位点下游内含子序列的系统分析揭示了富含U的基序和TIA1/TIAL1蛋白在可变剪接调控中的广泛作用。
Genome Res. 2008 Aug;18(8):1247-58. doi: 10.1101/gr.073155.107. Epub 2008 May 2.
7
MicroRNAs flex their muscles.微小RNA大显身手。
Trends Genet. 2008 Apr;24(4):159-66. doi: 10.1016/j.tig.2008.01.007. Epub 2008 Mar 5.
8
Myostatin promotes the terminal differentiation of embryonic muscle progenitors.肌生成抑制蛋白促进胚胎肌肉祖细胞的终末分化。
Genes Dev. 2008 Mar 1;22(5):668-81. doi: 10.1101/gad.454408.
9
Transcription factor Sp3 knockout mice display serious cardiac malformations.转录因子Sp3基因敲除小鼠表现出严重的心脏畸形。
Mol Cell Biol. 2007 Dec;27(24):8571-82. doi: 10.1128/MCB.01350-07. Epub 2007 Oct 8.
10
Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure.肥厚与心力衰竭过程中控制心肌肌球蛋白异构体转变的因素。
J Mol Cell Cardiol. 2007 Oct;43(4):388-403. doi: 10.1016/j.yjmcc.2007.07.045. Epub 2007 Jul 21.

内含子 microRNA 与其肌球蛋白宿主基因表达的脱偶联通过外显子跳跃实现。

Uncoupling of expression of an intronic microRNA and its myosin host gene by exon skipping.

机构信息

Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.

出版信息

Mol Cell Biol. 2010 Apr;30(8):1937-45. doi: 10.1128/MCB.01370-09. Epub 2010 Feb 12.

DOI:10.1128/MCB.01370-09
PMID:20154144
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2849460/
Abstract

The ancient MYH7b gene, expressed in striated muscle and brain, encodes a sarcomeric myosin and the intronic microRNA miR-499. We find that skipping of an exon introduces a premature termination codon in the transcript that downregulates MYH7b protein production without affecting microRNA expression. Among other genes, endogenous miR-499 targets the 3' untranslated region of the transcription factor Sox6, which in turn acts as a repressor of MYH7b transcriptional activity. Thus, concerted transcription and alternative splicing uncouple the level of expression of MYH7b and miR-499 when their coexpression is not required.

摘要

古老的 MYH7b 基因在横纹肌和大脑中表达,编码一个肌球蛋白和内含子 microRNA miR-499。我们发现,外显子的跳过会在转录本中引入一个过早终止密码子,从而下调 MYH7b 蛋白的产生,而不影响 microRNA 的表达。在其他基因中,内源性 miR-499 靶向转录因子 Sox6 的 3'非翻译区,而 Sox6 反过来又作为 MYH7b 转录活性的抑制剂。因此,当不需要它们的共表达时,协同转录和选择性剪接会使 MYH7b 和 miR-499 的表达水平解耦。