EGFR phosphorylates HDAC1 to regulate its expression and anti-apoptotic function.
EGFR phosphorylates HDAC1 to regulate its expression and anti-apoptotic function.
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DOI：
10.1038/s41419-021-03697-6
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发表时间：
2021-05-11
影响因子：
9
通讯作者：
Seto E
中科院分区：
文献类型：
--
作者：
Bahl S;Ling H;Acharige NPN;Santos-Barriopedro I;Pflum MKH;Seto E
HDAC1 is the prototypical human histone deacetylase (HDAC) enzyme responsible for catalyzing the removal of acetyl group from lysine residues on many substrate proteins. By deacetylating histones and non-histone proteins, HDAC1 has a profound effect on the regulation of gene transcription and many processes related to cell growth and cell death, including cell cycle progression, DNA repair, and apoptosis. Early studies reveal that, like most eukaryotic proteins, the functions and activities of HDAC1 are regulated by post-translational modifications. For example, serine phosphorylation of HDAC1 by protein kinase CK2 promotes HDAC1 deacetylase enzymatic activity and alters its interactions with proteins in corepressor complexes. Here, we describe an alternative signaling pathway by which HDAC1 activities are regulated. Specifically, we discover that EGFR activity promotes the tyrosine phosphorylation of HDAC1, which is necessary for its protein stability. A key EGFR phosphorylation site on HDAC1, Tyr72, mediates HDAC1’s anti-apoptotic function. Given that HDAC1 overexpression and EGFR activity are strongly related with tumor progression and cancer cell survival, HDAC1 tyrosine phosphorylation may present a possible target to manipulate HDAC1 protein levels in future potential cancer treatment strategies.
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影响因子：
11.8
作者：
Chou, Ruey-Hwang;Wang, Ying-Nai;Hsieh, Yi-Hsien;Li, Long-Yuan;Xia, Weiya;Chang, Wei-Chao;Chang, Ling-Chu;Cheng, Chien-Chia;Lai, Chien-Chen;Hsu, Jennifer L.;Chang, Wei-Jung;Chiang, Shu-Ya;Lee, Hong-Jen;Liao, Hsin-Wei;Chuang, Pei-Huan;Chen, Hui-Yu;Wang, Hung-Ling;Kuo, Sheng-Chu;Chen, Chung-Hsuan;Yu, Yung-Luen;Hung, Mien-Chie
通讯作者：
Hung, Mien-Chie
DOI：
10.1080/15384101.2015.1042634
发表时间：
2015
期刊：
Cell cycle (Georgetown, Tex.)
影响因子：
--
作者：
Bhaskara S
通讯作者：
Bhaskara S
吉非替尼诱导的表达突变体EGFR的NSCLC细胞系杀死需要BIM，并且可以通过BH3 Mimetics增强。
影响因子：
15.8
作者：
Cragg MS;Kuroda J;Puthalakath H;Huang DC;Strasser A
通讯作者：
Strasser A
BIM的诱导对于突变体EGFR依赖性肺腺癌中EGFR激酶抑制剂触发的凋亡至关重要。
影响因子：
15.8
作者：
Gong, Yixuan;Somwar, Romel;Politi, Katerina;Balak, Marissa;Chmielecki, Juliann;Jiang, Xuejun;Pao, William
通讯作者：
Pao, William
影响因子：
25
作者：
Kim, Jin Young;Shen, Siming;Dietz, Karen;He, Ye;Howell, Owain;Reynolds, Richard;Casaccia, Patrizia
通讯作者：
Casaccia, Patrizia