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p62

  • Open Access
    <span class="named-content genus-species" id="named-content-1">Mycobacterium tuberculosis</span> MmsA (Rv0753c) Interacts with STING and Blunts the Type I Interferon Response
    Research Article | Host-Microbe Biology
    Mycobacterium tuberculosis MmsA (Rv0753c) Interacts with STING and Blunts the Type I Interferon Response

    It is unclear how the type I IFN response is regulated by mycobacterial determinants. Here, we characterized the previously unreported role of M. tuberculosis MmsA in immunological regulation of type I IFN response by targeting the central adaptor STING in the DNA sensing pathway. We identified STING-interacting MmsA by coimmunoprecipitation-mass spectrometry-based (...

    Yifan Sun, Wei Zhang, Chunsheng Dong, Sidong Xiong
  • Open Access
    Pathogenesis of Human Papillomaviruses Requires the ATR/p62 Autophagy-Related Pathway
    Research Article | Molecular Biology and Physiology
    Pathogenesis of Human Papillomaviruses Requires the ATR/p62 Autophagy-Related Pathway

    High-risk human papillomaviruses (HPVs) infect epithelial cells and induce viral genome amplification upon differentiation. HPV proteins activate the ATR DNA damage repair pathway, and this is required for HPV genome amplification. In the present study, we show that HPV-induced ATR activation also leads to suppression of expression of inflammatory response genes. This suppression results from HPV-induced phosphorylation of the...

    Shiyuan Hong, Yan Li, Paul J. Kaminski, Jorge Andrade, Laimonis A. Laimins
  • Open Access
    CRISPR-Cas9 Screening of Kaposi’s Sarcoma-Associated Herpesvirus-Transformed Cells Identifies XPO1 as a Vulnerable Target of Cancer Cells
    Research Article | Host-Microbe Biology
    CRISPR-Cas9 Screening of Kaposi’s Sarcoma-Associated Herpesvirus-Transformed Cells Identifies XPO1 as a Vulnerable Target of Cancer Cells

    Using a model of oncogenic virus KSHV-driven cellular transformation of primary cells, we have performed a genome-wide CRISPR-Cas9 screening to identify vulnerable genes of cancer cells. This screening is unique in that this virus-induced oncogenesis model does not depend on any cellular genetic alterations and has matched primary and KSHV-transformed cells, which are not available for similar screenings in other types of cancer. We...

    Marion Gruffaz, Hongfeng Yuan, Wen Meng, Hui Liu, Sangsu Bae, Jin-Soo Kim, Chun Lu, Yufei Huang, Shou-Jiang Gao
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