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Cyclin E2‐ CDK 2 mediates SAMHD 1 phosphorylation to abrogate its restriction of HBV replication in hepatoma cells
Author(s) -
Hu Jie,
Qiao Miao,
Chen Yanmeng,
Tang Hua,
Zhang Wenlu,
Tang Dan,
Pi Sidie,
Dai Juan,
Tang Ni,
Huang Ailong,
Hu Yuan
Publication year - 2018
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 - 10.1002/1873-3468.13105
Subject(s) - samhd1 , cyclin dependent kinase , cyclin dependent kinase 6 , microbiology and biotechnology , cyclin a , cyclin dependent kinase 2 , cyclin dependent kinase 1 , phosphorylation , replication factor c , chemistry , biology , dna replication , cell cycle , eukaryotic dna replication , protein kinase a , biochemistry , cell , dna , reverse transcriptase , rna , gene
SAMHD 1 inhibits Hepatitis B virus ( HBV ) replication by reducing the intracellular dNTP levels. However, how SAMHD 1 phosphorylation is regulated to abrogate its restriction of HBV replication in hepatoma cells is poorly understood. Here, we show that HBV replication and SAMHD 1 phosphorylation levels are significantly reduced by knocking down cyclin‐dependent kinase ( CDK ) 2 expression or in the presence of a CDK 2 inhibitor. SAMHD 1 binds to CDK 2 in hepatocarcinoma cells, and this interaction does not require the HBV core protein. Furthermore, cyclin E2 participates in regulating viral replication through the CDK 2/ SAMHD 1 phosphorylation pathway in an HBV infection system. Collectively, our results provide evidence that CDK 2 has a greater role in regulating SAMHD 1 phosphorylation and HBV replication than CDK 1 or CDK 6.