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本文引用的文献

1
Modulation of exon skipping and inclusion by heterogeneous nuclear ribonucleoprotein A1 and pre-mRNA splicing factor SF2/ASF.异质性核糖核蛋白A1和前体mRNA剪接因子SF2/ASF对外显子跳跃和包含的调控
Mol Cell Biol. 1993 May;13(5):2993-3001. doi: 10.1128/mcb.13.5.2993-3001.1993.
2
The skipping of constitutive exons in vivo induced by nonsense mutations.无义突变在体内诱导组成型外显子跳跃。
Science. 1993 Jan 29;259(5095):680-3. doi: 10.1126/science.8430317.
3
Structural and functional diversity in the FGF receptor multigene family.成纤维细胞生长因子受体多基因家族中的结构与功能多样性。
Adv Cancer Res. 1993;60:1-41. doi: 10.1016/s0065-230x(08)60821-0.
4
Mutation of an RSV intronic element abolishes both U11/U12 snRNP binding and negative regulation of splicing.呼吸道合胞病毒内含子元件的突变会消除U11/U12核小核糖核蛋白的结合以及剪接的负调控。
Genes Dev. 1993 Oct;7(10):1926-36. doi: 10.1101/gad.7.10.1926.
5
Developmental localization of the splicing alternatives of fibroblast growth factor receptor-2 (FGFR2).成纤维细胞生长因子受体2(FGFR2)剪接异构体的发育定位
Dev Biol. 1993 Aug;158(2):475-86. doi: 10.1006/dbio.1993.1205.
6
The cardiac troponin T alternative exon contains a novel purine-rich positive splicing element.心肌肌钙蛋白T可变外显子包含一个新的富含嘌呤的正性剪接元件。
Mol Cell Biol. 1993 Jun;13(6):3660-74. doi: 10.1128/mcb.13.6.3660-3674.1993.
7
Control of BEK and K-SAM splice sites in alternative splicing of the fibroblast growth factor receptor 2 pre-mRNA.成纤维细胞生长因子受体2前体信使核糖核酸可变剪接中BEK和K-SAM剪接位点的调控
Mol Cell Biol. 1993 Sep;13(9):5461-8. doi: 10.1128/mcb.13.9.5461-5468.1993.
8
Polypurine sequences within a downstream exon function as a splicing enhancer.下游外显子内的聚嘌呤序列作为剪接增强子发挥作用。
Mol Cell Biol. 1994 Feb;14(2):1347-54. doi: 10.1128/mcb.14.2.1347-1354.1994.
9
General splicing factor SF2/ASF promotes alternative splicing by binding to an exonic splicing enhancer.通用剪接因子SF2/ASF通过与外显子剪接增强子结合来促进可变剪接。
Genes Dev. 1993 Dec;7(12B):2598-608. doi: 10.1101/gad.7.12b.2598.
10
A splicing enhancer in the human fibronectin alternate ED1 exon interacts with SR proteins and stimulates U2 snRNP binding.人类纤连蛋白可变ED1外显子中的一个剪接增强子与SR蛋白相互作用,并刺激U2 snRNP结合。
Genes Dev. 1993 Dec;7(12A):2405-17. doi: 10.1101/gad.7.12a.2405.

外显子序列TAGG可抑制剪接。

The exon sequence TAGG can inhibit splicing.

作者信息

Del Gatto F, Gesnel M C, Breathnach R

机构信息

INSERM U211, Institut de Biologie, Nantes, France.

出版信息

Nucleic Acids Res. 1996 Jun 1;24(11):2017-21. doi: 10.1093/nar/24.11.2017.

DOI:10.1093/nar/24.11.2017
PMID:8668531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC145892/
Abstract

The fibroblast growth factor receptor-2 gene contains a pair of alternative exons, K-SAM and BEK, which are spliced in a cell type specific manner. We have shown previously that a 10 nucleotide sequence within the K-SAM exon exerts a negative effect on K-SAM exon splicing independent of cell type. We demonstrate here that this sequence works autonomously, as it can repress splicing of a heterologous exon, the EIIIb alternative exon of the rat fibronectin gene. By introducing point mutations into the 10 nucleotide sequence, we have shown that the functional portion is limited to 4 nucleotides, TAGG, the dinucleotide AG of which is particularly important. This short sequence may participate in the control of splicing of exons carrying it, provided that they carry weak splice sites.

摘要

成纤维细胞生长因子受体-2基因包含一对可变外显子,即K-SAM和BEK,它们以细胞类型特异性方式进行剪接。我们之前已经表明,K-SAM外显子内的一个10个核苷酸的序列对K-SAM外显子的剪接产生负面影响,且与细胞类型无关。我们在此证明该序列具有自主作用,因为它可以抑制异源外显子(大鼠纤连蛋白基因的EIIIb可变外显子)的剪接。通过将点突变引入该10个核苷酸的序列,我们发现功能部分仅限于4个核苷酸,即TAGG,其中的二核苷酸AG尤为重要。这个短序列可能参与携带它的外显子的剪接控制,前提是这些外显子携带弱剪接位点。