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F11R 在缺氧时的表达受 RNA 编辑调控。

F11R expression upon hypoxia is regulated by RNA editing.

机构信息

Department of Pediatric Critical Care Medicine, Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel ; Sackler Medical School, Tel-Aviv University, Tel-Aviv, Israel.

出版信息

PLoS One. 2013 Oct 16;8(10):e77702. doi: 10.1371/journal.pone.0077702. eCollection 2013.

Abstract

F11R is a cell adhesion molecule found on the surface of human platelets. It plays a role in platelet aggregation, cell migration and cell proliferation. F11R is subjected to RNA editing, a post-transcriptional modification which affects RNA structure, stability, localization, translation and splicing. RNA editing in the 3'UTR of F11R and RNA levels are increased upon hypoxia. We therefore set to examine if RNA editing plays a role in the increase of F11R RNA seen upon hypoxic conditions. We show that ADAR1, but not ADAR2, takes part in the editing of F11R however editing alone is not sufficient for obtaining an elevation in RNA levels. In addition we show that hyper-edited mature mRNAs are retained in the nucleus and are associated with p54(nrb). We therefore conclude that hypoxia-induced edited RNAs of F11R are preferentially stabilized and accumulate in the nucleus preventing their export to the cytoplasm for translation. This mechanism may be used by additional proteins in the cell as part of the cell's effort to reduce metabolism upon hypoxic stress.

摘要

F11R 是一种细胞黏附分子,存在于人类血小板的表面。它在血小板聚集、细胞迁移和细胞增殖中发挥作用。F11R 经历 RNA 编辑,这是一种转录后修饰,影响 RNA 结构、稳定性、定位、翻译和剪接。F11R 的 3'UTR 中的 RNA 编辑和 RNA 水平在缺氧时增加。因此,我们着手研究 RNA 编辑是否在缺氧条件下 F11R RNA 增加中起作用。我们表明 ADAR1 而不是 ADAR2 参与 F11R 的编辑,但编辑本身不足以提高 RNA 水平。此外,我们表明,超编辑的成熟 mRNA 保留在细胞核中,并与 p54(nrb) 相关。因此,我们得出结论,缺氧诱导的 F11R 编辑 RNA 优先稳定并在细胞核中积累,防止其输出到细胞质进行翻译。这种机制可能被细胞中的其他蛋白质用作细胞在缺氧应激下降低代谢的一部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/901b/3797694/bd0f6020fee5/pone.0077702.g001.jpg

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