Conditional protein splicing of the Mycobacterium tuberculosis RecA intein in its native host
Author:
Funder
National Institutes of Health
Health Research Inc
Publisher
Springer Science and Business Media LLC
Link
https://www.nature.com/articles/s41598-024-71248-y.pdf
Reference75 articles.
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2. Singh, A. Guardians of the mycobacterial genome: A review on DNA repair systems in Mycobacterium tuberculosis. Microbiology (Reading) 163, 1740–1758. https://doi.org/10.1099/mic.0.000578 (2017).
3. Boshoff, H. I., Reed, M. B., Barry, C. E. 3rd. & Mizrahi, V. DnaE2 polymerase contributes to in vivo survival and the emergence of drug resistance in Mycobacterium tuberculosis. Cell 113, 183–193. https://doi.org/10.1016/s0092-8674(03)00270-8 (2003).
4. Stephanou, N. C. et al. Mycobacterial nonhomologous end joining mediates mutagenic repair of chromosomal double-strand DNA breaks. J. Bacteriol. 189, 5237–5246. https://doi.org/10.1128/JB.00332-07 (2007).
5. Sander, P. et al. Mycobacterium bovis BCG recA deletion mutant shows increased susceptibility to DNA-damaging agents but wild-type survival in a mouse infection model. Infect. Immun. 69, 3562–3568. https://doi.org/10.1128/IAI.69.6.3562-3568.2001 (2001).
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