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1
WT1 interacts with the splicing factor U2AF65 in an isoform-dependent manner and can be incorporated into spliceosomes.WT1以一种异构体依赖的方式与剪接因子U2AF65相互作用，并可被整合到剪接体中。
Genes Dev. 1998 Oct 15;12(20):3217-25. doi: 10.1101/gad.12.20.3217.
2
The Wilms' tumor gene WT1 can regulate genes involved in sex determination and differentiation: SRY, Müllerian-inhibiting substance, and the androgen receptor.肾母细胞瘤基因WT1可调控参与性别决定和分化的基因：SRY、苗勒管抑制物质和雄激素受体。
Clin Cancer Res. 1997 Dec;3(12 Pt 2):2571-80.
3
Products of alternatively spliced transcripts of the Wilms' tumor suppressor gene, wt1, have altered DNA binding specificity and regulate transcription in different ways.威尔姆斯肿瘤抑制基因wt1的可变剪接转录本产物具有改变的DNA结合特异性，并以不同方式调节转录。
Oncogene. 1995 Feb 2;10(3):415-22.
4
Expression in Xenopus oocytes shows that WT1 binds transcripts in vivo, with a central role for zinc finger one.非洲爪蟾卵母细胞中的表达表明，WT1在体内与转录本结合，锌指1起核心作用。
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5
Wilms' tumor gene WT1 promotes homologous recombination-mediated DNA damage repair.肾母细胞瘤基因WT1促进同源重组介导的DNA损伤修复。
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6
Frasier syndrome is caused by defective alternative splicing of WT1 leading to an altered ratio of WT1 +/-KTS splice isoforms.弗雷泽综合征是由WT1基因的异常可变剪接引起的，导致WT1 +/-KTS剪接异构体的比例发生改变。
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7
Truncated WT1 mutants alter the subnuclear localization of the wild-type protein.截短的WT1突变体改变了野生型蛋白的亚核定位。
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8
Donor splice-site mutations in WT1 are responsible for Frasier syndrome.WT1基因的供体剪接位点突变是弗雷泽综合征的病因。
Nat Genet. 1997 Dec;17(4):467-70. doi: 10.1038/ng1297-467.
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The speckling domain of the Wilms tumor suppressor WT1 overlaps with the transcriptional repression domain.肾母细胞瘤抑制因子WT1的斑点结构域与转录抑制结构域重叠。
FEBS Lett. 2001 Apr 6;494(1-2):69-73. doi: 10.1016/s0014-5793(01)02313-4.
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WT1 interacts with the splicing protein RBM4 and regulates its ability to modulate alternative splicing in vivo.WT1与剪接蛋白RBM4相互作用，并在体内调节其调控可变剪接的能力。
Exp Cell Res. 2006 Oct 15;312(17):3379-88. doi: 10.1016/j.yexcr.2006.07.008. Epub 2006 Jul 25.

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Urinary Podocyte Count as a Potential Routine Laboratory Test for Glomerular Disease: A Novel Method Using Liquid-Based Cytology and Immunoenzyme Staining.尿足细胞计数作为肾小球疾病的一种潜在常规实验室检测方法：一种使用液基细胞学和免疫酶染色的新方法。
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Altered VEGF Splicing Isoform Balance in Tumor Endothelium Involves Activation of Splicing Factors Srpk1 and Srsf1 by the Wilms' Tumor Suppressor Wt1.肿瘤内皮中血管内皮生长因子剪接异构体平衡的改变涉及 Wilms 瘤抑制因子 WT1 通过激活剪接因子 Srpk1 和 Srsf1。
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Polymorphisms in the Wilms Tumor Gene Are Associated With Interindividual Variations in Rubella Virus-Specific Cellular Immunity After Measles-Mumps-Rubella II Vaccination.Wilms 瘤基因多态性与麻疹-腮腺炎-风疹二联疫苗接种后风疹病毒特异性细胞免疫的个体间差异相关。
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本文引用的文献

1
Wilms' tumor 1 and Dax-1 modulate the orphan nuclear receptor SF-1 in sex-specific gene expression.肾母细胞瘤1和Dax-1在性别特异性基因表达中调节孤儿核受体SF-1。
Cell. 1998 May 1;93(3):445-54. doi: 10.1016/s0092-8674(00)81172-1.
2
A cooperative interaction between U2AF65 and mBBP/SF1 facilitates branchpoint region recognition.U2AF65与mBBP/SF1之间的协同相互作用有助于分支点区域识别。
Genes Dev. 1998 Mar 15;12(6):858-67. doi: 10.1101/gad.12.6.858.
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Transcription units as RNA processing units.作为RNA加工单位的转录单位。
Genes Dev. 1997 Dec 15;11(24):3279-85. doi: 10.1101/gad.11.24.3279.
4
Donor splice-site mutations in WT1 are responsible for Frasier syndrome.WT1基因的供体剪接位点突变是弗雷泽综合征的病因。
Nat Genet. 1997 Dec;17(4):467-70. doi: 10.1038/ng1297-467.
5
U2AF65 recruits a novel human DEAD box protein required for the U2 snRNP-branchpoint interaction.U2AF65招募一种新型人类DEAD盒蛋白，该蛋白是U2 snRNP与分支点相互作用所必需的。
Genes Dev. 1997 Jul 15;11(14):1864-72. doi: 10.1101/gad.11.14.1864.
6
A protein related to splicing factor U2AF35 that interacts with U2AF65 and SR proteins in splicing of pre-mRNA.一种与剪接因子U2AF35相关的蛋白质，在pre-mRNA剪接过程中与U2AF65和SR蛋白相互作用。
Nature. 1997 Jul 24;388(6640):397-400. doi: 10.1038/41137.
7
The dynamics of a pre-mRNA splicing factor in living cells.活细胞中前体mRNA剪接因子的动力学
Nature. 1997 May 29;387(6632):523-7. doi: 10.1038/387523a0.
8
Targeting of U2AF65 to sites of active splicing in the nucleus.U2AF65定位于细胞核中活跃剪接的位点。
J Cell Biol. 1997 Jun 2;137(5):975-87. doi: 10.1083/jcb.137.5.975.
9
Cross-intron bridging interactions in the yeast commitment complex are conserved in mammals.酵母前体信使核糖核蛋白体复合物中的交叉内含子桥接相互作用在哺乳动物中保守存在。
Cell. 1997 May 2;89(3):403-12. doi: 10.1016/s0092-8674(00)80221-4.
10
A clinical overview of WT1 gene mutations.WT1基因突变的临床概述。
Hum Mutat. 1997;9(3):209-25. doi: 10.1002/(SICI)1098-1004(1997)9:3<209::AID-HUMU2>3.0.CO;2-2.

WT1以一种异构体依赖的方式与剪接因子U2AF65相互作用，并可被整合到剪接体中。

WT1 interacts with the splicing factor U2AF65 in an isoform-dependent manner and can be incorporated into spliceosomes.

作者信息

Davies R C, Calvio C, Bratt E, Larsson S H, Lamond A I, Hastie N D

机构信息

Medical Research Council (MRC) Human Genetics Unit, Western General Hospital, Edinburgh EH4 2XU, UK.

出版信息

Genes Dev. 1998 Oct 15;12(20):3217-25. doi: 10.1101/gad.12.20.3217.

DOI:10.1101/gad.12.20.3217
PMID:9784496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC317218/
Abstract

WT1 is essential for normal kidney development, and genetic alterations are associated with Wilms' tumor, Denys Drash (DDS), and Frasier syndromes. Although generally considered a transcription factor this study has revealed that WT1 interacts with an essential splicing factor, U2AF65, and associates with the splicing machinery. WT1 is alternatively spliced and isoforms that include three amino acids, KTS, show stronger interaction with U2AF65 in vitro and better colocalization with splicing factors in vivo. Interestingly a mutation associated with DDS enhanced both -KTS WT1 binding to U2AF65 and splicing-factor colocalization. These data illustrate the functional importance of WT1 isoforms and suggest that WT1 plays a role in pre-mRNA splicing.

摘要

WT1对于正常肾脏发育至关重要，基因改变与威尔姆斯瘤、迪尼-德拉斯（DDS）综合征和弗雷泽综合征相关。尽管通常被认为是一种转录因子，但本研究表明WT1与一种关键的剪接因子U2AF65相互作用，并与剪接机制相关联。WT1存在可变剪接，包含三个氨基酸KTS的异构体在体外与U2AF65的相互作用更强，在体内与剪接因子的共定位更好。有趣的是，与DDS相关的一种突变增强了-KTS WT1与U2AF65的结合以及与剪接因子的共定位。这些数据说明了WT1异构体的功能重要性，并表明WT1在mRNA前体剪接中发挥作用。