http://www.cnr.it/ontology/cnr/individuo/prodotto/ID295826
hnRNP L inhibits CD44 V10 exon splicing through interacting with its upstream intron (Articolo in rivista)
- Type
- Label
- hnRNP L inhibits CD44 V10 exon splicing through interacting with its upstream intron (Articolo in rivista) (literal)
- Anno
- 2015-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.bbagrm.2015.01.004. (literal)
- Alternative label
Loh TJ, Cho S, Moon H, Jang HN, Williams DR, Jung DW, Kim IC, Ghigna C, Biamonti G, Zheng X, Shen H. (2015)
hnRNP L inhibits CD44 V10 exon splicing through interacting with its upstream intron
in Biochimica et biophysica acta. Gene regulatory mechanisms (Print)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Loh TJ, Cho S, Moon H, Jang HN, Williams DR, Jung DW, Kim IC, Ghigna C, Biamonti G, Zheng X, Shen H. (literal)
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- School of life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Republic of Korea
Department of Biological Sciences, Chonnam National University, Gwangju 500-757, Republic of Korea
Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, via Abbiategrasso 207, 27100 Pavia, Italy (literal)
- Titolo
- hnRNP L inhibits CD44 V10 exon splicing through interacting with its upstream intron (literal)
- Abstract
- CD44 is a complex cell adhesion molecule that mediates communication and adhesion between adjacent cells as well as between cells and the extracellular matrix. CD44 pre-mRNA produces various mRNA isoforms through alternative splicing of 20 exons, among which exons 1-5 (C1-C5) and 16-20 (C6-C10) are constant exons, whereas exons 6-15 (V1-V10) are variant exons. CD44 V10 exon has important roles in tumor progression and Hodgkin lymphoma. Here we show that increased expression of hnRNP L inhibits V10 exon splicing of CD44 pre-mRNA, whereas reduced expression of hnRNP L promotes V10 exon splicing. In addition, hnRNP L also promotes V10 splicing of endogenous CD44 pre-mRNA. Through mutation analysis, we demonstrate that the effects of hnRNP L on V10 splicing are abolished when the CA-rich sequence on the upstream intron of V10 exon is disrupted. However, hnRNP L effects are stronger if more CA-repeats are provided. Furthermore, we show that hnRNP L directly contacts the CA-rich sequence. Importantly, we provide evidences that hnRNP L inhibits U2AF65 binding on the upstream Py tract of V10 exon. Our results reveal that hnRNP L is a new regulator for CD44 V10 exon splicing. (literal)
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