Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader–Willi syndrome-Reference-Cited by-同舟云学术

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Targeting the histone methyltransferase G9a activates imprinted genes and improves survival of a mouse model of Prader–Willi syndrome

Published:2016-12-26 Issue:2 Volume:23 Page:213-222
ISSN:1078-8956
Container-title:Nature Medicine
language:en
Short-container-title:Nat Med

Author:

Kim Yuna,Lee Hyeong-Min,Xiong Yan,Sciaky Noah,Hulbert Samuel W,Cao Xinyu,Everitt Jeffrey I,Jin Jian,Roth Bryan L,Jiang Yong-hui

Publisher

Springer Science and Business Media LLC

Subject

General Biochemistry, Genetics and Molecular Biology,General Medicine

Link

http://www.nature.com/articles/nm.4257.pdf

Reference57 articles.

1. Cassidy, S.B. & Driscoll, D.J. Prader–Willi syndrome. Eur. J. Hum. Genet. 17, 3–13 (2009).

2. Buiting, K. Prader-Willi syndrome and Angelman syndrome. Am. J. Med. Genet. C. Semin. Med. Genet. 154C, 365–376 (2010).

3. Sahoo, T. et al. Prader-Willi phenotype caused by paternal deficiency for the HBII-85 C/D box small nucleolar RNA cluster. Nat. Genet. 40, 719–721 (2008).

4. de Smith, A.J. et al. A deletion of the HBII-85 class of small nucleolar RNAs (snoRNAs) is associated with hyperphagia, obesity and hypogonadism. Hum. Mol. Genet. 18, 3257–3265 (2009).

5. Duker, A.L. et al. Paternally inherited microdeletion at 15q11.2 confirms a significant role for the SNORD116 C/D box snoRNA cluster in Prader-Willi syndrome. Eur. J. Hum. Genet. 18, 1196–1201 (2010).

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