Author

M. Brocard

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Microbiology· 3

Signature Assays, Organisms & Methods

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Research Focus:host-pathogen & immune response· 3 Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:metagenomics· 1

Frequent Co-Authors

N. Locker· 3 shared J. Lu· 2 shared A. Ruggieri· 1 shared B. Hall· 1 shared B. S. Hall· 1 shared C. Moller-Levet· 1 shared D. Beste· 1 shared F. Sorgeloos· 1 shared

Activity by Year

2018-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersMicrobiology

N. Locker

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Murine Norovirus infection results in anti-inflammatory response downstream of amino acids depletion in macrophages

M. Brocard, J. Lu, B. S. Hall, K. Borah, C. Moller-Levet, F. Sorgeloos, D. Beste, I. G. Goodfellow, N. Locker

This study shows that murine norovirus induces metabolic stress in macrophages, leading to anti-inflammatory responses through amino acid depletion and GCN2/ATF2 signaling, rather than a typical innate immune response.

bioRxiv · Apr 22, 2021Microbiology

Infectious bronchitis virus regulates cellular stress granule signaling

M. J. Brownsword, N. Doyle, M. Brocard, N. Locker, H. J. Maier

This study investigates how infectious bronchitis virus modulates cellular stress granule signaling and translational repression during infection.

bioRxiv · Oct 28, 2019Microbiology

Norovirus infection results in assembly of virus-specific G3BP1 granules and evasion of eIF2α signaling.

M. Brocard, V. Iadevaia, P. Klein, B. Hall, G. Lewis, J. Lu, J. Burke, R. Parker, A. Ruggieri, I. Goodfellow, N. Locker

This study shows that norovirus infection leads to the formation of virus-specific granules and disrupts eIF2α signaling to evade host stress responses.

bioRxiv · Dec 10, 2018 · PreprintMicrobiology