Sensing and responding to cytosolic viruses invasions: An orchestra of kaleidoscopic ubiquitinations

Liu, Xing; Wang, Qiang; Pan, Ying; Wang, Chen

doi:10.1016/j.cytogfr.2015.03.001

Cited by 20 publications

(13 citation statements)

References 87 publications

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“…The significance of STING phosphorylation at additional serine sites is under evaluation, but they are thought to have a role in the control of STING degradation 17 . Furthermore, several studies have now indicated that STING is ubiquitylated on a number of lysine residues 26 .…”

Section: The Sting Signalling Pathwaymentioning

confidence: 99%

STING: infection, inflammation and cancer

2015

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The rapid detection of microbial agents is essential for the effective initiation of host defence mechanisms against infection. Understanding how cells detect cytosolic DNA to trigger innate immune gene transcription has important implications — not only for comprehending the immune response to pathogens but also for elucidating the causes of autoinflammatory disease involving the sensing of self-DNA and the generation of effective antitumour adaptive immunity. The discovery of the STING (stimulator of interferon genes)-controlled innate immune pathway, which mediates cytosolic DNA-induced signalling events, has recently provided important insights into these processes, opening the way for the development of novel immunization regimes, as well as therapies to treat autoinflammatory disease and cancer.

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Section: The Sting Signalling Pathwaymentioning

confidence: 99%

STING: infection, inflammation and cancer

2015

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“…The activity of RING-type ubiquitin-protein ligases relies on their RING-domains which contain conserved cysteine and histidine residues essential for recruiting the E2 ubiquitin-conjugating enzymes [27]. Several RING-type E3 ubiquitin-protein ligases have been demonstrated in the regulation of antiviral responses [28]. For example, RNF5 regulates antiviral responses by targeting MITA for degradation after viral infection [29], whereas TRIM32 targets MITA for K63-linked ubiquitination to positively modulate type I IFN production [30].…”

Section: Introductionmentioning

confidence: 99%

RNF90 negatively regulates cellular antiviral responses by targeting MITA for degradation

et al. 2020

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Mediator of IRF3 activation (MITA, also named as STING/ERIS/MPYS/TMEM173), is essential to DNA virus-or cytosolic DNA-triggered innate immune responses. In this study, we demonstrated the negative regulatory role of RING-finger protein (RNF) 90 in innate immune responses targeting MITA. RNF90 promoted K48-linked ubiquitination of MITA and its proteasome-dependent degradation. Overexpression of RNF90 inhibited HSV-1-or cytosolic DNA-induced immune responses whereas RNF90 knockdown had the opposite effects. Moreover, RNF90-deficient bone marrow-derived dendritic cells (BMDCs), bone marrow-derived macrophages (BMMs) and mouse embryonic fibroblasts (MEFs) exhibited increased DNA virus-or cytosolic DNA-triggered signaling and RNF90 deficiency protected mice from DNA virus infection. Taken together, our findings suggested a novel function of RNF90 in innate immunity. OPEN ACCESS Citation: Yang B, Liu Y, Cui Y, Song D, Zhang G, Ma S, et al. (2020) RNF90 negatively regulates cellular antiviral responses by targeting MITA for degradation. PLoS Pathog 16(3): e1008387.

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“…Great progress has recently been made in understanding cytosolic DNA recognition systems and corresponding STING signaling [101,102]; however, many questions remain answered. Recent studies have uncovered several potential DNA-binding proteins that sense the presence of microbial DNA in the cytoplasm and consequently induce type I IFN production.…”

Section: Discussionmentioning

confidence: 98%