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Release of Human Cytomegalovirus from latency by a KAP1/TRIM28 phosphorylation switch

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NIAID Data Ecosystem2026-03-11 收录
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https://www.ncbi.nlm.nih.gov/sra/SRP034016
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资源简介:
A new actor of HCMV latency is unveiled, where KAP1 protein binds to viral genome to recruit SetDB1 and trigger H3K9 trimethylation. A switch of phosphorylation state mediated by mTOR leads to lytic replication, opening new approaches to curtail CMV infection but also to purge the virus from organ transplants. Overall design: Analyses of transcriptional profiles and chromatin state in KAP1 WT and KO (or KD) cells
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2019-09-24
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