B. F. Usher
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View article: Nucleotidyltransferase toxin MenT extends aminoacyl acceptor ends of serine tRNAs to control Mycobacterium tuberculosis growth
Nucleotidyltransferase toxin MenT extends aminoacyl acceptor ends of serine tRNAs to control Mycobacterium tuberculosis growth Open
Toxins of toxin-antitoxin systems use diverse mechanisms to inhibit bacterial growth. In this study, we characterize the translation inhibitor toxin MenT3 of Mycobacterium tuberculosis , the bacterium responsible for tuberculosis in humans…
View article: Inducible auto-phosphorylation regulates a widespread family of nucleotidyltransferase toxins
Inducible auto-phosphorylation regulates a widespread family of nucleotidyltransferase toxins Open
Nucleotidyltransferases (NTases) control diverse physiological processes, including RNA modification, DNA replication and repair, and antibiotic resistance. The Mycobacterium tuberculosis NTase toxin family, MenT, modifies tRNAs to block t…
View article: Nucleotidyltransferase toxin MenT targets and extends the aminoacyl acceptor ends of serine tRNAs<i>in vivo</i>to control<i>Mycobacterium tuberculosis</i>growth
Nucleotidyltransferase toxin MenT targets and extends the aminoacyl acceptor ends of serine tRNAs<i>in vivo</i>to control<i>Mycobacterium tuberculosis</i>growth Open
Toxins of toxin-antitoxin systems use diverse mechanisms to control bacterial growth and represent attractive therapeutic targets to fight pathogens. In this study, we characterized the translation inhibitor toxin MenT3 of Mycobacterium tu…
View article: MenT nucleotidyltransferase toxins extend tRNA acceptor stems and can be inhibited by asymmetrical antitoxin binding
MenT nucleotidyltransferase toxins extend tRNA acceptor stems and can be inhibited by asymmetrical antitoxin binding Open
View article: Crystal structure of the anti-CRISPR repressor Aca2
Crystal structure of the anti-CRISPR repressor Aca2 Open
Bacteria use adaptive CRISPR-Cas immune mechanisms to protect from invasion by bacteriophages and other mobile genetic elements. In response, bacteriophages and mobile genetic elements have co-evolved anti-CRISPR proteins to inhibit the ba…
View article: Tuberculosis drug discovery: an in-house toxin blocks pathogenic bacterial growth
Tuberculosis drug discovery: an in-house toxin blocks pathogenic bacterial growth Open
Tuberculosis causes more deaths worldwide every year than any other infectious disease, except COVID-19. Today, its treatment is getting increasingly challenging due to the rise of antibiotic-resistant variants of disease-causing bacteria.…
View article: A nucleotidyltransferase toxin inhibits growth of <i>Mycobacterium tuberculosis</i> through inactivation of tRNA acceptor stems
A nucleotidyltransferase toxin inhibits growth of <i>Mycobacterium tuberculosis</i> through inactivation of tRNA acceptor stems Open
The human pathogen Mycobacterium tuberculosis produces a toxin that can stall bacterial growth by blocking the activity of tRNAs.
View article: Antitoxin autoregulation of <i>M. tuberculosis</i> toxin-antitoxin expression through negative cooperativity arising from multiple inverted repeat sequences
Antitoxin autoregulation of <i>M. tuberculosis</i> toxin-antitoxin expression through negative cooperativity arising from multiple inverted repeat sequences Open
Toxin-antitoxin systems play key roles in bacterial adaptation, including protection from antibiotic assault and infection by bacteriophages. The type IV toxin-antitoxin system AbiE encodes a DUF1814 nucleotidyltransferase-like toxin, and …