Epigenetics at the base of alternative splicing changes that promote colorectal cancer
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....
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2017
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219738_v127_n9_p3281_Kornblihtt http://hdl.handle.net/20.500.12110/paper_00219738_v127_n9_p3281_Kornblihtt |
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paper:paper_00219738_v127_n9_p3281_Kornblihtt2023-06-08T14:44:51Z Epigenetics at the base of alternative splicing changes that promote colorectal cancer 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 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. 2017 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219738_v127_n9_p3281_Kornblihtt http://hdl.handle.net/20.500.12110/paper_00219738_v127_n9_p3281_Kornblihtt |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
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 |
| spellingShingle |
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 Epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| topic_facet |
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 |
| description |
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. |
| title |
Epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| title_short |
Epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| title_full |
Epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| title_fullStr |
Epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| title_full_unstemmed |
Epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| title_sort |
epigenetics at the base of alternative splicing changes that promote colorectal cancer |
| publishDate |
2017 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219738_v127_n9_p3281_Kornblihtt http://hdl.handle.net/20.500.12110/paper_00219738_v127_n9_p3281_Kornblihtt |
| _version_ |
1768546006345973760 |