Author

Matthew Knight

University of California, Berkeley

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

Biology Disciplines

Click to filter author papers

Microbiology· 1 Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 2 Organism:bacteria (other)· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1 Research Focus:host-pathogen & immune response· 1 Organism:mouse· 1 Research Focus:variant calling· 1

Frequent Co-Authors

Adam M. DeutschbaueriD· 1 shared Chantal A. Coles· 1 shared David F. SavageiD· 1 shared Elizabeth M. Gibbs· 1 shared Hans K. CarlsoniD· 1 shared Hualan LiuiD· 1 shared Jason D. White· 1 shared Katie A. LieniD· 1 shared

Activity by Year

2018-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperMicrobiology

Adam M. DeutschbauerORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Random barcode transposon-site sequencing in Mycobacterium tuberculosis reveals the functions of uncharacterized genes

Kayla M. Dinshaw, Katie A. Lien, Matthew Knight, Sorel V. Yigma Ouonkap, Hualan Liu, David F. Savage, Hans K. Carlson, Adam M. Deutschbauer, Sarah A. Stanley

This study uses random barcode transposon-site sequencing in Mycobacterium tuberculosis to identify gene functions, revealing novel phenotypes and metabolic pathways.

bioRxiv · Nov 13, 2025 · PreprintMicrobiology

Benfotiamine reduces pathology and improves muscle function in mdx mice.

Keryn G. Woodman, Chantal A. Coles, Su L Toulson, Elizabeth M. Gibbs, Matthew Knight, Matthew McDonagh, Rachelle H. Crosbie-Watson, Shireen R. Lamandé, Jason D. White

Benfotiamine reduces dystrophic pathology and improves muscle function in mdx mice by decreasing inflammation and increasing utrophin/dystrophin complex expression.

bioRxiv · Mar 25, 2018 · PreprintPhysiology