REST and the RESTless: in stem cells and beyond.
REST and the RESTless: in stem cells and beyond.
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DOI：
10.2217/fnl.09.1
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发表时间：
2009
期刊：
影响因子：
1.3
通讯作者：
Gopalakrishnan V
中科院分区：
文献类型：
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作者：
Gopalakrishnan V
自从最初发现阻遏元件 (RE)-1 沉默转录因子 (REST)（也称为神经元限制性沉默因子）作为神经元分化的负调节因子以来，它一直与胚胎干细胞多能性的维持、自我更新以及非神经细胞有丝分裂保真度的调节等新过程有关。 REST 表达和活性受到细胞中转录和转录后机制的严格控制，并且其水平或功能的扰动与各种病理状态相关。 REST 通过以上下文相关的方式与多种细胞辅助因子相互作用，对靶基因表达产生差异性影响。然而，人们对微环境对 REST 介导的基因表达调控的影响知之甚少。这篇综述将介绍我们目前对 REST 信号传导的理解，重点关注其与非编码 RNA 和新型相互作用伙伴的新兴联系，以及其在胚胎干细胞自我更新、细胞可塑性和肿瘤发生/肿瘤抑制中的作用。
Since its original discovery as a negative regulator of neuronal differentiation, the repressor element (RE)-1 silencing transcription factor (REST), also known as the neuron-restrictive silencer factor, has been implicated in novel processes such as maintenance of embryonic stem cell pluripotency and self-renewal and regulation of mitotic fidelity in non-neural cells. REST expression and activity is tightly controlled by transcriptional and post-transcriptional mechanisms in a cell and developmental stage-specific manner and perturbations in its levels or function are associated with various pathological states. REST differentially influences target-gene expression through interaction with a wide variety of cellular cofactors in a context-dependent manner. However, the influence of the microenvironment on REST-mediated regulation of gene expression is poorly understood. This review will present our current understanding of REST signaling with a greater focus on its emerging ties with noncoding RNAs and novel interacting partners, as well as its roles in embryonic stem cell self-renewal, cellular plasticity and oncogenesis/tumor suppression.