Xu, Wenqi
Li, Jiahui
Rong, Bowen
Zhao, Bin
Wang, Mei
Dai, Ruofei
Chen, Qilong
Liu, Hang
Gu, Zhongkai
Liu, Shuxian
Guo, Rui
Shen, Hongjie http://orcid.org/0000-0001-9771-7988
Wu, Feizhen http://orcid.org/0000-0002-1265-9887
Lan, Fei http://orcid.org/0000-0002-8559-7146
Article History
First Online: 22 November 2019
Change Date: 9 December 2019
Change Type: Correction
Change Details: The author would like to add the below information in this correction. A similar study from Chao Lu group was published online on 5 September 2019 in Nature, entitled “The histone mark H3K36me2 recruits DNMT3A and shapes the intergenic DNA methylation landscape” (Weinberg et al., 2019). Although both the studies reported the preferential recognition of H3K36me2 by DNMT3A PWWP, ours in addition uncovered a stimulation function by such interaction on the activity of DNMT3A. On the disease connections, we used a NSD2 gain-of-function model which led to the discovery of potential therapeutic implication of DNA inhibitors in the related cancers, while the other study only used NSD1 and DNMT3A loss-of-function models.
Change Date: 9 December 2019
Change Type: Correction
Change Details: The author would like to add the below information in this correction. A similar study from Chao Lu group was published online on 5 September 2019 in Nature, entitled ���The histone mark H3K36me2 recruits DNMT3A and shapes the intergenic DNA methylation landscape��� (Weinberg et al., 2019). Although both the studies reported the preferential recognition of H3K36me2 by DNMT3A PWWP, ours in addition uncovered a stimulation function by such interaction on the activity of DNMT3A. On the disease connections, we used a NSD2 gain-of-function model which led to the discovery of potential therapeutic implication of DNA inhibitors in the related cancers, while the other study only used NSD1 and DNMT3A loss-of-function models.