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Abstract:

Chromatin modification influences gene expression by either repressing or activating genes, depending on the specific histone mark. Chromatin structure can also influence alternative splicing of transcripts; however, the mechanisms by which epigenetic marks influence splicing are poorly understood. A report in the current issue of the JCI highlights the biological importance of the coordinated control of alternative pre-mRNA splicing by chromatin structure and transcriptional elongation. Yuan et al. found that mutation of the histone methyl transferase SEDT2 affects alternative splicing fates of several key regulatory genes, including those involved in Wnt signaling. As a consequence, loss of SEDT2 in the intestine aggravated Wnt/β-catenin signaling effects, thereby leading to colorectal cancer.

Registro:

Documento: Artículo
Título:Epigenetics at the base of alternative splicing changes that promote colorectal cancer
Autor:Kornblihtt, A.R.
Filiación:Universidad de Buenos Aires (UBA), Facultad de Ciencias Exactas y Naturales, Departamento de Fisiología, Biología Molecular y Celular and CONICET-UBA, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), Buenos Aires, 1428, Argentina
Palabras clave:beta catenin; histone methyltransferase; histone methyltransferase SEDT2; messenger RNA precursor; unclassified drug; Wnt protein; RNA precursor; alternative RNA splicing; chromatin structure; colorectal cancer; epigenetics; human; nonhuman; nonsense mediated mRNA decay; priority journal; regulator gene; Review; transcription elongation; Wnt signaling; colorectal tumor; genetic epigenesis; genetics; RNA splicing; Alternative Splicing; Colorectal Neoplasms; Epigenesis, Genetic; Humans; RNA Precursors; RNA Splicing
Año:2017
Volumen:127
Número:9
Página de inicio:3281
Página de fin:3283
DOI: http://dx.doi.org/10.1172/JCI96497
Título revista:Journal of Clinical Investigation
Título revista abreviado:J. Clin. Invest.
ISSN:00219738
CODEN:JCINA
CAS:RNA Precursors
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219738_v127_n9_p3281_Kornblihtt

Referencias:

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  • Barash, Y., Deciphering the splicing code (2010) Nature, 465 (7294), pp. 53-59
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  • Tilgner, H., Deep sequencing of subcellular RNA fractions shows splicing to be predominantly co-transcriptional in the human genome but inefficient for lncRNAs (2012) Genome Res, 22 (9), pp. 1616-1625
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  • Luco, R.F., Pan, Q., Tominaga, K., Blencowe, B.J., Pereira-Smith, O.M., Misteli, T., Regulation of alternative splicing by histone modifications (2010) Science, 327 (5968), pp. 996-1000
  • Yuan, H., Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis (2017) J Clin Invest, 127 (9), pp. 3375-3391
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Citas:

---------- APA ----------
(2017) . Epigenetics at the base of alternative splicing changes that promote colorectal cancer. Journal of Clinical Investigation, 127(9), 3281-3283.
http://dx.doi.org/10.1172/JCI96497
---------- CHICAGO ----------
Kornblihtt, A.R. "Epigenetics at the base of alternative splicing changes that promote colorectal cancer" . Journal of Clinical Investigation 127, no. 9 (2017) : 3281-3283.
http://dx.doi.org/10.1172/JCI96497
---------- MLA ----------
Kornblihtt, A.R. "Epigenetics at the base of alternative splicing changes that promote colorectal cancer" . Journal of Clinical Investigation, vol. 127, no. 9, 2017, pp. 3281-3283.
http://dx.doi.org/10.1172/JCI96497
---------- VANCOUVER ----------
Kornblihtt, A.R. Epigenetics at the base of alternative splicing changes that promote colorectal cancer. J. Clin. Invest. 2017;127(9):3281-3283.
http://dx.doi.org/10.1172/JCI96497