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Mmu-miR-702 functions as an anti-apoptotic mirtron by mediating ATF6 inhibition in mice.
Zhang, Wei-Guang; Chen, Lin; Dong, Qin; He, Juan; Zhao, Han-Dong; Li, Feng-Lan; Li, Hui.
Afiliación
  • Zhang WG; Department of Biochemistry and Molecular Biology, Basic Medical Science College, Harbin Medical University, Harbin 150081, China.
Gene ; 531(2): 235-42, 2013 Dec 01.
Article en En | MEDLINE | ID: mdl-24035931
MicroRNAs (miRNAs) are a group of endogenous, small, noncoding RNAs that function as key post-transcriptional regulators. miRNAs are involved in many biological processes including apoptosis. In this study, mouse miR-702 (mmu-miR-702), a mirtron derived from the 13th intron of the Plod3 gene, was identified as a regulator of anti-apoptosis. mmu-miR-702 was down-regulated after treatment with the apoptosis-inducer isoproterenol both in vivo and in vitro. According to over-expression experiments, mmu-miR-702 inhibited apoptosis as well as the expression levels of a subset of apoptosis-related genes including activating transcription factor 6 (ATF6). An interaction between mmu-miR-702 and the ATF6 3'-UTR binding site was confirmed using luciferase reporter and western blot assays. This is the first report of ATF6 interaction with miRNA. Although the possible existence of miR-702 in the human genome is low, our results indicate that mirtrons also participate in the process of apoptosis and may provide a novel study strategy for apoptosis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Apoptosis / MicroARNs / Factor de Transcripción Activador 6 Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Gene Año: 2013 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Apoptosis / MicroARNs / Factor de Transcripción Activador 6 Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Gene Año: 2013 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos