关注RNA解旋 - Suppr

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Eye on RNA unwinding.

作者信息

Brow David A

出版信息

Nat Struct Mol Biol. 2009 Jan;16(1):7-8. doi: 10.1038/nsmb0109-7.

DOI:10.1038/nsmb0109-7

PMID:19125166

Abstract

摘要

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Eye on RNA unwinding.关注RNA解旋

Nat Struct Mol Biol. 2009 Jan;16(1):7-8. doi: 10.1038/nsmb0109-7.

ATP-dependent unwinding of U4/U6 snRNAs by the Brr2 helicase requires the C terminus of Prp8.Brr2解旋酶对U4/U6小核RNA进行ATP依赖的解旋需要Prp8的C末端。

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PRPF mutations are associated with generalized defects in spliceosome formation and pre-mRNA splicing in patients with retinitis pigmentosa.PRPF 突变与视网膜色素变性患者剪接体形成和前体 mRNA 剪接的普遍缺陷有关。

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Mutations in the pre-mRNA splicing-factor genes PRPF3, PRPF8, and PRPF31 in Spanish families with autosomal dominant retinitis pigmentosa.西班牙常染色体显性视网膜色素变性家族中前体mRNA剪接因子基因PRPF3、PRPF8和PRPF31的突变

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Retinitis Pigmentosa Mutations in Bad Response to Refrigeration 2 (Brr2) Impair ATPase and Helicase Activity.视网膜色素变性中对冷藏反应不佳2（Brr2）的突变会损害ATP酶和解旋酶活性。

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Protein 61K, encoded by a gene (PRPF31) linked to autosomal dominant retinitis pigmentosa, is required for U4/U6*U5 tri-snRNP formation and pre-mRNA splicing.由与常染色体显性视网膜色素变性相关的基因（PRPF31）编码的蛋白质61K，是U4/U6*U5三小核核糖核蛋白形成和前体信使核糖核酸剪接所必需的。

EMBO J. 2002 Mar 1;21(5):1148-57. doi: 10.1093/emboj/21.5.1148.

Brr2 plays a role in spliceosomal activation in addition to U4/U6 unwinding.除了解开U4/U6之外，Brr2在剪接体激活中也发挥作用。

Nucleic Acids Res. 2015 Mar 31;43(6):3286-97. doi: 10.1093/nar/gkv062. Epub 2015 Feb 10.

Splicing factor Prp8 governs U4/U6 RNA unwinding during activation of the spliceosome.剪接因子Prp8在剪接体激活过程中调控U4/U6 RNA解旋。

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Functional contacts with a range of splicing proteins suggest a central role for Brr2p in the dynamic control of the order of events in spliceosomes of Saccharomyces cerevisiae.与一系列剪接蛋白的功能性接触表明，Brr2p在酿酒酵母剪接体中事件顺序的动态控制中起核心作用。

Genetics. 2001 Apr;157(4):1451-67. doi: 10.1093/genetics/157.4.1451.

Association of PAP-1 and Prp3p, the products of causative genes of dominant retinitis pigmentosa, in the tri-snRNP complex.PAP-1和Prp3p（显性视网膜色素变性致病基因的产物）在三小核核糖核蛋白复合体中的关联。

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本文引用的文献

ATP-dependent unwinding of U4/U6 snRNAs by the Brr2 helicase requires the C terminus of Prp8.Brr2解旋酶对U4/U6小核RNA进行ATP依赖的解旋需要Prp8的C末端。

Nat Struct Mol Biol. 2009 Jan;16(1):42-8. doi: 10.1038/nsmb.1535. Epub 2008 Dec 21.

Is the spliceosome a ribonucleoprotein enzyme?剪接体是一种核糖核蛋白酶吗？

Nat Struct Mol Biol. 2008 Dec;15(12):1235-7. doi: 10.1038/nsmb1208-1235.

Localization of Prp8, Brr2, Snu114 and U4/U6 proteins in the yeast tri-snRNP by electron microscopy.通过电子显微镜对酵母三小核核糖核蛋白中Prp8、Brr2、Snu114和U4/U6蛋白进行定位。

Nat Struct Mol Biol. 2008 Nov;15(11):1206-12. doi: 10.1038/nsmb.1506. Epub 2008 Oct 26.

Structure and function of an RNase H domain at the heart of the spliceosome.剪接体核心区域核糖核酸酶H结构域的结构与功能

EMBO J. 2008 Nov 5;27(21):2929-40. doi: 10.1038/emboj.2008.209. Epub 2008 Oct 9.

Structural elucidation of a PRP8 core domain from the heart of the spliceosome.剪接体核心部位PRP8核心结构域的结构解析

Nat Struct Mol Biol. 2008 Nov;15(11):1199-205. doi: 10.1038/nsmb.1505. Epub 2008 Oct 2.

Crystal structure of the beta-finger domain of Prp8 reveals analogy to ribosomal proteins.Prp8蛋白β-指状结构域的晶体结构显示出与核糖体蛋白的相似性。

Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13817-22. doi: 10.1073/pnas.0805960105. Epub 2008 Sep 8.

A conformational rearrangement in the spliceosome sets the stage for Prp22-dependent mRNA release.剪接体中的构象重排为依赖Prp22的mRNA释放奠定了基础。

Mol Cell. 2008 Jun 20;30(6):743-54. doi: 10.1016/j.molcel.2008.05.003.

"Nought may endure but mutability": spliceosome dynamics and the regulation of splicing.“唯有变化才是永恒”：剪接体动力学与剪接调控

Mol Cell. 2008 Jun 20;30(6):657-66. doi: 10.1016/j.molcel.2008.04.013.

A role for ubiquitin in the spliceosome assembly pathway.泛素在剪接体组装途径中的作用。

Nat Struct Mol Biol. 2008 May;15(5):444-51. doi: 10.1038/nsmb.1401. Epub 2008 Apr 20.

prp8 mutations that cause human retinitis pigmentosa lead to a U5 snRNP maturation defect in yeast.导致人类视网膜色素变性的prp8突变会在酵母中引发U5 snRNP成熟缺陷。

Nat Struct Mol Biol. 2007 Nov;14(11):1077-83. doi: 10.1038/nsmb1303. Epub 2007 Oct 14.

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