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
A microfluidic-based genetic screen to identify microbial virulence factors that inhibit dendritic cell migration
Laura M. McLaughlin,Laura M. McLaughlin,Hui Xu,Sarah Carden,Samantha Fisher,Monique Reyes,Sarah C. Heilshorn,Denise M. Monack +7 more
TL;DR: A positive selection microfluidic-based genetic screen that allows us to identify Salmonella virulence factors that manipulate dendritic cell (DC) migration within stable, linear chemokine gradients is developed.
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Cloning of Bordetella bronchiseptica urease genes and analysis of colonization by a urease‐negative mutant strain in a guinea‐pig model
Denise M. Monack,Stanley Falkow +1 more
TL;DR: It is demonstrated that urease is not essential for B. bronchiseptica colonization of the guinea‐pig respiratory and digestive tracts.
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Coordinate actions of innate immune responses oppose those of the adaptive immune system during Salmonella infection of mice
Andrew Hotson,Smita Gopinath,Monica Nicolau,Anna Khasanova,Rachel Finck,Denise M. Monack,Garry P. Nolan +6 more
TL;DR: System-wide manipulation of neutrophil numbers revealed that neutrophils regulated signal transducer and activator of transcription (STAT) signaling in B cells during infection, which enacts a coordinated response when faced with complex environmental and pathogenic perturbations.
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Delayed activation of host innate immune pathways in streptozotocin-induced diabetic hosts leads to more severe disease during infection with Burkholderia pseudomallei.
TL;DR: Poor glycaemic control impaired innate responses during the early stages of B. pseudomallei acute infection, contributing to the increased susceptibility of STZ‐induced diabetics to this fatal disease.
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Escalating Threat Levels of Bacterial Infection Can Be Discriminated by Distinct MAPK and NF-κB Signaling Dynamics in Single Host Cells.
TL;DR: A combined, single-cell approach reveals that NF-κB and MAPK signaling dynamics are sufficient to discriminate between pathogen-associated molecular patterns (PAMPs) versus bacteria, extracellular versus intracellular bacteria, pathogenic versus non-pathogenic bacteria, and the presence or absence of features indicating an active intrACEllular bacterial infection.