Author

S. K C

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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Biochemistry· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Organism:human· 1 Assay:imaging· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

A. K B· 1 shared A. K. R· 1 shared A. Madhavan· 1 shared B. Abraham· 1 shared B. M· 1 shared M. P P· 1 shared N. P· 1 shared R. R J· 1 shared

Activity by Year

2020-2025 · peak 1/yr

Co-Author Collaboration Network

9 top collaborators · 18 mutual co-author links

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1 shared paperBiochemistry

A. K B

Mutual co-authors in cluster

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2 papers

Recent·Most cited

ESAT-6 of Mycobacterium tuberculosis downregulates cofilin1, leads to filamentous actin enrichment and reduces the phagosome acidification in infected macrophages, which are partially reversed by a single methionine mutation

M. P P, R. R J, S. K C, S. Mundayoor

Tuberculosis · Dec 1, 2025Peer-reviewedImmunology

Acetylation of isoniazid - a novel mechanism of isoniazid resistance in Mycobacterium tuberculosis

A. K B, A. Madhavan, B. Abraham, B. M, S. K C, N. P, A. K. R

This study identifies Rv2170 as an acetyltransferase that inactivates isoniazid by acetylation, providing a novel mechanism for isoniazid resistance in Mycobacterium tuberculosis.

bioRxiv · Feb 10, 2020Biochemistry