Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis-Reference-Cited by-同舟云学术

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Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis

Published:2017-08-21 Issue:9 Volume:127 Page:3375-3391
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:

Author:

Yuan Huairui,Li Ni,Fu Da,Ren Jiale,Hui Jingyi,Peng Junjie,Liu Yongfeng,Qiu Tong,Jiang Min,Pan Qiang,Han Ying,Wang Xiaoming,Li Qintong^ORCID,Qin Jun

Funder

the Strategic Priority Research Program of the Chinese Academy of Sciences

the National Natural Science Foundation of China

the National Key Basic Research Program

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Link

https://www.jci.org/articles/view/94292/files/pdf

Reference67 articles.

1. A decade of exploring the cancer epigenome — biological and translational implications

2. Genome-wide maps of chromatin state in pluripotent and lineage-committed cells

3. Dynamic histone H3 methylation during gene induction: HYPB/Setd2 mediates all H3K36 trimethylation

4. Histone H3 lysine 36 methyltransferase Hypb/Setd2 is required for embryonic vascular remodeling

5. Understanding the language of Lys36 methylation at histone H3

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