HDAC11 regulates type I interferon signaling through defatty-acylation of SHMT2

Proceedings of the National Academy of Sciences of the United States of America - Tập 116 Số 12 - Trang 5487-5492 - 2019
Ji Cao1,2,3, Lei Sun4, Pornpun Aramsangtienchai2, Nicole A. Spiegelman2, Xiaoyu Zhang2, Weishan Huang5, Edward Seto4, Hening Lin2,6
1College of Pharmaceutical Sciences, Zhejiang University, 310058 Hangzhou, China
2Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853
3Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, 310058 Hangzhou, China;
4George Washington University Cancer Center, Washington, DC 20037;
5Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and
6Howard Hughes Medical Institute, Cornell University, Ithaca, NY 14853

Tóm tắt

Significance

HDAC11 is the only class IV member of the histone deacetylase (HDAC) family, and very little is known about its biological function. The work here reveals its efficient and physiologically relevant activity. The regulation of SHMT2 and interferon signaling expands the known biological function of protein lysine fatty acylation, which has only recently started to be appreciated. Furthermore, a compelling molecular mechanism is proposed to connect HDAC11 to immune response. The finding opens exciting opportunities to develop HDAC11-specific inhibitors to treat human diseases that would benefit from increased type I interferon signaling, such as viral infection, multiple sclerosis, and cancer.

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Thông tin xuất bản

Proceedings of the National Academy of Sciences of the United States of America

Tập 116 Số 12

5487-5492

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