http://www.cnr.it/ontology/cnr/individuo/prodotto/ID287341
SRSF2 promotes splicing and transcription of exon 11 included isoform in Ron proto-oncogene (Articolo in rivista)
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- SRSF2 promotes splicing and transcription of exon 11 included isoform in Ron proto-oncogene (Articolo in rivista) (literal)
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- 2014-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.bbagrm.2014.09.003 (literal)
- Alternative label
Moon H, Cho S, Loh TJ, Oh HK, Jang HN, Zhou J, Kwon YS, Liao DJ, Jun Y, Eom S, Ghigna C, Biamonti G, Green MR, Zheng X, Shen H. (2014)
SRSF2 promotes splicing and transcription of exon 11 included isoform in Ron proto-oncogene
in Biochimica et biophysica acta. Gene regulatory mechanisms (Online)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Moon H, Cho S, Loh TJ, Oh HK, Jang HN, Zhou J, Kwon YS, Liao DJ, Jun Y, Eom S, Ghigna C, Biamonti G, Green MR, Zheng X, Shen H. (literal)
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- School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 500-712, South Korea; JiangSu Key Laboratory of Neuroregeneration, Nantong University, Nantong, China; Department of Bioscience and Biotechnology, Sejong University, Seoul, 143-747, South Korea; Hormel Institute, University of Minnesota, Austin, MN, United States; Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, via Abbiategrasso 207, Pavia, 27100, Italy; Howard Hughes Medical Institute and Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, United States (literal)
- Titolo
- SRSF2 promotes splicing and transcription of exon 11 included isoform in Ron proto-oncogene (literal)
- Abstract
- The product of proto-oncogene Ron is a human receptor for the macrophage-stimulating protein (MSP). Upon activation, Ron is able to induce cell dissociation, migration and matrix invasion. Exon 11 skipping of Ron pre-mRNA produces Ron?165 protein that is constitutively active even in the absence of its ligand. Here we show that knockdown of SRSF2 promotes the decrease of exon 11 inclusion, whereas overexpression of SRSF2 promotes exon 11 inclusion. We demonstrate that SRSF2 promotes exon 11 inclusion through splicing and transcription procedure. We also present evidence that reduced expression of SRSF2 induces a decrease in the splicing of both introns 10 and 11; by contrast, overexpression of SRSF2 induces an increase in the splicing of introns 10 and 11. Through mutation analysis, we show that SRSF2 functionally targets and physically interacts with CGAG sequence on exon 11. In addition, we reveal that the weak strength of splice sites of exon 11 is not required for the function of SRSF2 on the splicing of Ron exon 11. Our results indicate that SRSF2 promotes exon 11 inclusion of Ron proto-oncogene through targeting exon 11. Our study provides a novel mechanism by which Ron is expressed. (literal)
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