Yi Wang
University of Hong Kong
19 Papers
4 Citations
Yi Wang is an academic researcher from University of Hong Kong. The author has contributed to research in topics: Medicine & Chromatin. The author has an hindex of 13, co-authored 15 publications. Previous affiliations of Yi Wang include Li Ka Shing Faculty of Medicine, University of Hong Kong & University of Science and Technology of China.
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Papers
SIRT6 regulates TNF-α secretion through hydrolysis of long-chain fatty acyl lysine
Hong Jiang,Saba Khan,Yi Wang,Guillaume Charron,Bin He,Carlos Sebastian,Jintang Du,Raymond J. Kim,Eva J. Ge,Raul Mostoslavsky,Howard C. Hang,Quan Hao,Hening Lin +12 more
TL;DR: It is shown that human SIRT6 efficiently removes long-chain fatty acyl groups, such as myristoyl, from lysine residues and promotes the secretion of tumour necrosis factor-α (TNF-α) by removing the fatty acy modification on K19 and K20 of TNF- α.
Identification of ‘erasers’ for lysine crotonylated histone marks using a chemical proteomics approach
Xiucong Bao,Yi Wang,Xin Li,Xiao-Meng Li,Zheng Liu,Tangpo Yang,Chi F.at Wong,Jiangwen Zhang,Quan Hao,Xiang D.avid Li +9 more
TL;DR: It is found that Sirt1, Sirt2, and Sirt3 can catalyze the hydrolysis of lysine crotonylated histone peptides and proteins and functions as a decrotonylase to regulate histone Kcr dynamics and gene transcription in living cells.
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Lysine benzoylation is a histone mark regulated by SIRT2
TL;DR: It is demonstrated that histone Kbz marks are associated with gene expression and have physiological relevance distinct from histone acetylation, and SIRT2, a NAD+-dependent protein deacetylase, removes histoneKbz both in vitro and in vivo.
Lamin A Is an Endogenous SIRT6 Activator and Promotes SIRT6-Mediated DNA Repair
TL;DR: It is reported that lamin A is an endogenous activator of SIRT6 and facilitates chromatin localization of Sirt6 upon DNA damage and reveals a critical role for lamination A in regulating SIRT 6 activities, suggesting that defects in SIRT8 functions contribute to impaired DNA repair and accelerated aging in HGPS.
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