D
Denise M. Monack
Researcher at Stanford University
Publications - 152
Citations - 24804
Denise M. Monack is an academic researcher from Stanford University. The author has contributed to research in topics: Innate immune system & Inflammasome. The author has an hindex of 73, co-authored 145 publications receiving 22245 citations. Previous affiliations of Denise M. Monack include Rocky Mountain Laboratories & University of California, Los Angeles.
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Journal ArticleDOI
Shedding light on Salmonella carriers
TL;DR: Recent advances in molecular profiling of human carriers and the use of animal models to identify potential host and bacterial genes involved in the establishment of the carrier state are described.
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Salmonella pathogenicity island 2-dependent macrophage death is mediated in part by the host cysteine protease caspase-1.
TL;DR: It is shown here that the human pathogen Salmonella typhi also triggers both rapid, caspase‐1‐dependent and delayed cell death in human monocytes and that IL‐1β is released during both SPI1‐ and SPI2‐dependent macrophage killing.
Journal ArticleDOI
NLR-mediated control of inflammasome assembly in the host response against bacterial pathogens.
Igor E. Brodsky,Denise M. Monack +1 more
TL;DR: This review will discuss the recent developments regarding caspase-1 activation in response to bacterial infection, cross-talk between caspASE-1 and other pathways involved in regulating cell death, and recent findings that a number of bacterial pathogens possess mechanisms to inhibit casp enzyme activation.
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The Salmonella SPI2 effector SseI mediates long-term systemic infection by modulating host cell migration.
Laura M. McLaughlin,Gregory R. Govoni,Christiane Gerke,Smita Gopinath,Kaitian Peng,Grace Laidlaw,Yueh-hsiu Chien,Ha-Won Jeong,Zhigang Li,Matthew D. Brown,David B. Sacks,Denise M. Monack +11 more
TL;DR: It is demonstrated that the bacterial effector protein SseI inhibits normal host cell migration, which ultimately counteracts the ability of the host to clear systemic bacteria.
Journal ArticleDOI
Cutting Edge: Inflammasome Activation in Primary Human Macrophages Is Dependent on Flagellin.
TL;DR: Human Naip functions to activate the inflammasome in response to flagellin, similar to murine Naip5/6.