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EZH2 phosphorylation regulates Tat‐induced HIV‐1 transactivation via ROS/Akt signaling pathway
Author(s) -
Zhang Hong-Sheng,
Liu Yang,
Wu Tong-Chao,
Du Guang-Yuan,
Zhang Feng-Juan
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.11.033
Subject(s) - transactivation , ezh2 , protein kinase b , phosphorylation , gene silencing , chemistry , transfection , biology , microbiology and biotechnology , cancer research , epigenetics , gene expression , biochemistry , gene
EZH2 plays a major role in HIV‐1 latency, however, the molecular linkage between Tat‐induced HIV‐1 transactivation and EZH2 activity is not fully understood. It was shown Tat induced HIV‐1 transactivation through inhibiting EZH2 activity. Tat decreased the levels of H3K27me3 and EZH2 occupy at the long terminal repeat (LTR) of HIV‐1. We further showed for the first time that transfected with Tat construct resulted in an increase in phosphorylated EZH2 (p‐EZH2), mediated by active Akt. ROS/Akt‐dependent p‐EZH2 was correlated with Tat‐induced transactivation. Our study reveals that novel mechanisms allow Tat‐induced HIV‐1 transactivation by ROS/Akt‐dependent downregulating the EZH2 epigenetic silencing machinery.