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Downstream targets of ATR in CIN612 HPV-positive cells

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NIAID Data Ecosystem2026-03-12 收录
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https://www.ncbi.nlm.nih.gov/sra/SRP238473
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资源简介:
High-risk human papillomaviruses (HPVs) constitutively activate the ataxia telangiectasia and Rad3-related (ATR) DNA damage response pathway for their replication. Although ATR has many reported functions, knowledge of how it regulates viral replication is limited. Most studies regarding ATR function focus on its roles in cell survival and initiation of DNA damage response. In this study, we examined whether the transcriptional regulatory properties directed by ATR are critical for HPV pathogenesis, and if so which downstream targets are important. Using RNA-seq approaches, we observed that ATR knockdown increases expression of many inflammatory genes. This mechanism is dependent on the p62/GATA4 signaling pathway. Overall design: CIN612 cells were transduced with ATR shRNAs and selected for the stable lines, before the analysis
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2020-09-01
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