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Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition.
Mol Cell. 2005 Aug 19; 19(4):475-84.MC

Abstract

Fas exon 6 can be included or skipped to generate mRNAs encoding, respectively, a membrane bound form of the receptor that promotes apoptosis or a soluble isoform that prevents programmed cell death. We report that the apoptosis-inducing protein TIA-1 promotes U1 snRNP binding to the 5' splice site of intron 6, which in turn facilitates exon definition by enhancing U2AF binding to the 3' splice site of intron 5. The polypyrimidine tract binding protein (PTB) promotes exon skipping by binding to an exonic splicing silencer and inhibiting the association of U2AF and U2 snRNP with the upstream 3' splice site, without affecting recognition of the downstream 5' splice site by U1. Remarkably, U1 snRNP-mediated recognition of the 5' splice site is required both for efficient U2AF binding and for U2AF inhibition by PTB. We propose that TIA-1 and PTB regulate Fas splicing and possibly Fas-mediated apoptosis by targeting molecular events that lead to exon definition.

Authors+Show Affiliations

Centre de Regulació Genòmica, Passeig Marítim 37-49, 08003 Barcelona, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16109372

Citation

Izquierdo, José María, et al. "Regulation of Fas Alternative Splicing By Antagonistic Effects of TIA-1 and PTB On Exon Definition." Molecular Cell, vol. 19, no. 4, 2005, pp. 475-84.
Izquierdo JM, Majós N, Bonnal S, et al. Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition. Mol Cell. 2005;19(4):475-84.
Izquierdo, J. M., Majós, N., Bonnal, S., Martínez, C., Castelo, R., Guigó, R., Bilbao, D., & Valcárcel, J. (2005). Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition. Molecular Cell, 19(4), 475-84.
Izquierdo JM, et al. Regulation of Fas Alternative Splicing By Antagonistic Effects of TIA-1 and PTB On Exon Definition. Mol Cell. 2005 Aug 19;19(4):475-84. PubMed PMID: 16109372.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition. AU - Izquierdo,José María, AU - Majós,Nuria, AU - Bonnal,Sophie, AU - Martínez,Concepción, AU - Castelo,Robert, AU - Guigó,Roderic, AU - Bilbao,Daniel, AU - Valcárcel,Juan, PY - 2004/12/23/received PY - 2005/05/12/revised PY - 2005/06/15/accepted PY - 2005/8/20/pubmed PY - 2005/10/12/medline PY - 2005/8/20/entrez SP - 475 EP - 84 JF - Molecular cell JO - Mol Cell VL - 19 IS - 4 N2 - Fas exon 6 can be included or skipped to generate mRNAs encoding, respectively, a membrane bound form of the receptor that promotes apoptosis or a soluble isoform that prevents programmed cell death. We report that the apoptosis-inducing protein TIA-1 promotes U1 snRNP binding to the 5' splice site of intron 6, which in turn facilitates exon definition by enhancing U2AF binding to the 3' splice site of intron 5. The polypyrimidine tract binding protein (PTB) promotes exon skipping by binding to an exonic splicing silencer and inhibiting the association of U2AF and U2 snRNP with the upstream 3' splice site, without affecting recognition of the downstream 5' splice site by U1. Remarkably, U1 snRNP-mediated recognition of the 5' splice site is required both for efficient U2AF binding and for U2AF inhibition by PTB. We propose that TIA-1 and PTB regulate Fas splicing and possibly Fas-mediated apoptosis by targeting molecular events that lead to exon definition. SN - 1097-2765 UR - https://www.unboundmedicine.com/medline/citation/16109372/Regulation_of_Fas_alternative_splicing_by_antagonistic_effects_of_TIA_1_and_PTB_on_exon_definition_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1097-2765(05)01418-8 DB - PRIME DP - Unbound Medicine ER -