RNA-directed transcriptional gene silencing and activation in human cells.
RNA-directed transcriptional gene silencing and activation in human cells.
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DOI：
10.1089/oli.2009.0212
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发表时间：
2009-12
期刊：
影响因子：
--
通讯作者：
Morris KV
中科院分区：
文献类型：
--
作者：
Morris KV
基因表达的明显丧失或不受控制的获得在某种程度上存在于几乎每一种折磨人类的疾病中。从癌症到HIV-1，基因表达的失控或缺失在人类疾病中普遍存在。在转录水平上对基因表达进行特异性控制的方法可能具有逆转或减少疾病病理的潜力。在过去的几年里，研究人员已经开发出利用小的反义非编码RNA来特异性沉默转录的方法。直到最近才确定了通过引入这些小RNA来调节人类细胞转录的内源性分子途径。观察结果表明，长反义非编码RNA作为人类细胞中转录的内源性表观遗传调节因子，从而解释了为什么早期观察到小反义RNA通过靶基因座处的定向表观遗传变化沉默转录。小调控RNA可以打开或关闭基因转录的作用机制将被讨论，作为有一天可能开发出调节基因转录和改善特定疾病状况的治疗方法的证据。
The overt loss or uncontrolled gain of gene expression is found at some level in virtually every malady afflicting humans. From cancer to HIV-1, the uncontrolled expression or loss of gene expression is prevalent in human diseases. Approaches toward the specific control of gene expression at the transcriptional level could have the potential to revert or reduce disease pathologies. Over the last several years, researchers have developed methodologies that utilize small antisense non-coding RNAs to specifically silence transcription. Only recently has the endogenous molecular pathway usurped by the introduction of these small RNAs to regulate transcription in human cells been defined. Observations suggest that long antisense non-coding RNAs function as the endogenous epigenetic regulators of transcription in human cells, thus explaining why small antisense RNAs were observed early on to silence transcription via directed epigenetic changes at the target loci. The mechanism of action whereby small regulatory RNAs can either turn gene transcription on or off will be discussed as evidence that one day it may be possible to develop therapeutics to regulate gene transcription and ameliorate particular disease conditions.
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DOI：
10.1073/pnas.0808830105
发表时间：
2008-10-21
影响因子：
11.1
作者：
Kim, Daniel H.;Saetrom, Pal;Rossi, John J.
通讯作者：
Rossi, John J.
影响因子：
56.9
作者：
Kapranov, Philipp;Cheng, Jill;Gingeras, Thomas R.
通讯作者：
Gingeras, Thomas R.
影响因子：
16.8
作者：
Janowski, Bethany A.;Huffman, Kenneth E.;Corey, David R.
通讯作者：
Corey, David R.
影响因子：
11.4
作者：
MATZKE, MA;PRIMIG, M;MATZKE, AJM
通讯作者：
MATZKE, AJM
影响因子：
14.9
作者：
Hawkins PG;Santoso S;Adams C;Anest V;Morris KV
通讯作者：
Morris KV