Author

C.-Y. Cheung

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· 4

Signature Assays, Organisms & Methods

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Research Focus:drug response / drug discovery· 4 Organism:human· 3 Assay:bulk RNA-seq· 2 Approach:experimental assay· 2 Approach:genetic perturbation / CRISPR· 2 Assay:ATAC-seq· 1 Research Focus:cell type annotation· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

G. Cook· 2 shared G. M. Cook· 2 shared M. B. McNeil· 2 shared N. J. Waller· 2 shared A. Al-Zubaidi· 1 shared A. L. Peterson· 1 shared B. Nijagal· 1 shared G. Taiaroa· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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2 shared papersMicrobiology

G. Cook

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

KatG inactivation generates vulnerabilities in isoniazid resistant strains of Mycobacterium tuberculosis

X. Wang, W. J. Jowsey, C.-Y. Cheung, N. E. Seeto, N. J. Waller, M. T. Chrisp, A. L. Peterson, B. Nijagal, P. C. Fineran, G. M. Cook, S. A. Jackson, M. B. McNeil

The paper identifies vulnerabilities in isoniazid-resistant Mycobacterium tuberculosis strains by analyzing metabolic and transcriptional changes in katG mutants.

bioRxiv · Dec 7, 2023 · PreprintMicrobiology

The evolution of antibiotic resistance is associated with collateral drug phenotypes in Mycobacterium tuberculosis

N. J. Waller, C.-Y. Cheung, G. Cook, M. B. McNeil

This study shows that drug resistance in M. tuberculosis can lead to collateral sensitivity to unrelated drugs, offering new strategies to combat drug-resistant strains.

bioRxiv · Oct 31, 2022 · PreprintMicrobiology

Multiplexed transcriptional repression identifies a network of bactericidal interactions between mycobacterial respiratory complexes

M. McNeil, H. Ryburn, J. Tirados, C.-Y. Cheung, G. Cook

This study uses CRISPRi to identify synthetic lethal interactions between mycobacterial respiratory complexes, revealing key bactericidal combinations.

bioRxiv · Sep 18, 2021Microbiology

RNase HI depletion strongly potentiates cell killing by rifampicin in mycobacteria

A. Al-Zubaidi, C.-Y. Cheung, G. M. Cook, G. Taiaroa, V. Mizrahi, J. S. Lott, S. S. Dawes

This paper shows that reducing RNase HI activity in mycobacteria increases sensitivity to rifampicin, suggesting RNase HI as a target for new antibiotics.

bioRxiv · Jul 14, 2021Microbiology