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Publicacion

Titulo:	Sam68 Regulates the Alternative Splicing of Survivin DEx3
Autores:	GAYTAN-CERVANTES J GONZALEZ-TORRES C VILMA ARACELI MALDONADO LAGUNAS ZAMPEDRI C GISELA CEBALLOS CANCINO JORGE MELÉNDEZ ZAJGLA
Tipo de Licencia:	http://creativecommons.org/licenses/by/4.0
Fecha de Publicación:	27 de Junio de 2017
Resumen:	Messenger RNA alternative splicing (AS) regulates the expression of a variety of genes involved in both physiological and pathological processes. AS of the antiapoptotic and proliferation-associated survivin (BIRC5) gene generates six isoforms, which regulate key aspects of cancer initiation and progression. One of the isoforms is survivin DEx3, in which the exclusion of exon 3 generates a unique carboxyl terminus with specific antiapoptotic functions. This isoform is highly expressed in advanced stages of breast and cervical tumours. Therefore, understanding the mechanisms that regulate survivin DEx3 mRNA AS is clearly important. To this end, we designed a minigene (M), and in combination with a series of deletions and site-directed mutations, we determined that the first 22 bp of exon 3 contain cis-acting elements that enhance the exclusion of exon 3 to generate the survivin DEx3 mRNA isoform. Furthermore, using pull-down assays, we discovered that Sam68 is a possible trans-acting factor that binds to this region and regulates exon 3 splicing. This result was corroborated using a cell line in which the Sam68 binding site in the survivin gene was mutated with the Crispr/Cas system. This work provides the first clues regarding the regulation of survivin DEx3 mRNA splicing.
Editorial:	JOURNAL OF BIOLOGICAL CHEMISTRY
Idioma:	Ingles
Palabras Clave:
URL:	https://repositorio.inmegen.gob.mx/record/408

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