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Mitoxosome: a mitochondrial platform for cross-talk between cellular stress and antiviral signaling

期刊

IMMUNOLOGICAL REVIEWS
卷 243, 期 -, 页码 215-234

出版社

WILEY
DOI: 10.1111/j.1600-065X.2011.01038.x

关键词

viral infection; reactive oxygen species; Toll-like receptors/pattern recognition receptors; apoptosis/autophagy; inflammation; mitochondria

资金

  1. National Institutes of Health (NIH) [AI054359, AI062428, AI064705, AI083242]
  2. Burroughs Wellcome Fund
  3. NIH Ruth L. Kirschstein National Research Service [F31 AG039163]

向作者/读者索取更多资源

Evidence is accumulating that the mitochondria form an integral platform from which innate signaling takes place. Recent studies revealed that the mitochondria are shaping the innate response to intracellular pathogens, and mitochondrial function is modulating and being modulated by innate immune signaling. Further, cell biologic analyses have uncovered the dynamic relocalization of key components involved in cytosolic viral recognition and signaling to the mitochondria, as well as the mobilization of mitochondria to the sites of viral replication. In this review, we provide an integrated view of how cellular stress and signals following cytosolic viral recognition are intimately linked and coordinated at the mitochondria. We incorporate recent findings into our current understanding of the role of mitochondrial function in antiviral immunity and suggest the existence of a 'mitoxosome', a mitochondrial oxidative signalosome where multiple pathways of viral recognition and cellular stress converge on the surface of the mitochondria to facilitate a coordinated antiviral response.

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