PABPN1 关闭了可变 poly(A) 位点。
PABPN1 shuts down alternative poly(A) sites.
机构信息
mRNA Regulation and Development, Institute of Human Genetics, CNRS UPR1142, Montpellier Cedex 5, France.
出版信息
Cell Res. 2012 Oct;22(10):1419-21. doi: 10.1038/cr.2012.86. Epub 2012 May 29.
Abstract
Although overlooked for many years, alternative cleavage and polyadenylation (APA) is now emerging as a major mechanism of gene regulation. A recent study identifies poly(A)-binding protein nuclear 1 (PABPN1), a general factor of polyadenylation, as a suppressor of alternative poly(A) sites.
摘要
虽然多年来一直被忽视，但选择性剪接和多聚腺苷酸化 (APA) 现在正成为一种主要的基因调控机制。最近的一项研究确定了多聚腺苷酸结合蛋白核 1 (PABPN1)，一种多聚腺苷酸化的通用因子，作为选择性多聚腺苷酸化位点的抑制剂。
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The poly(A)-binding protein nuclear 1 suppresses alternative cleavage and polyadenylation sites.多聚（A）结合蛋白核 1 抑制可变剪接和多聚腺苷酸化位点。
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Ending the message: poly(A) signals then and now.结束信息：多聚（A）信号，过去和现在。
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The nuclear poly(A)-binding protein interacts with the exosome to promote synthesis of noncoding small nucleolar RNAs.核多聚（A）结合蛋白与核酶体相互作用，促进非编码小核仁 RNA 的合成。
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