ArticleMolecular microbiology2017
Chemical activation of adenylyl cyclase Rv1625c inhibits growth of Mycobacterium tuberculosis on cholesterol and modulates intramacrophage signaling.
Article in Molecular microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- An adenylyl cyclase switch reroutes carbon from growth to virulence lipids inbioRxiv : the preprint server for biology · 2026Article
- Phosphoglucomutase A-mediated metabolic adaptation is essential for antibiotic and disease persistence inmSystems · 2025Article
- A Review of Antibacterial Candidates with New Modes of Action.ACS infectious diseases · 2024Review
- Exploiting cAMP signaling in Mycobacterium tuberculosis for drug discovery.Trends in microbiology · 2024Review
- Article
- Review
- Mycobacterial phosphodiesterase Rv0805 is a virulence determinant and its cyclic nucleotide hydrolytic activity is required for propionate detoxification.Molecular microbiology · 2023Article
- Cyclic AMP-Mediated Inhibition of Cholesterol Catabolism inAntimicrobial agents and chemotherapy · 2023Article
- Structure ofeLife · 2022Article
- GSK2556286 Is a Novel Antitubercular Drug Candidate EffectiveAntimicrobial agents and chemotherapy · 2022Article
- Pharmacological and genetic activation of cAMP synthesis disrupts cholesterol utilization in Mycobacterium tuberculosis.PLoS pathogens · 2022Article
- Targeting Mycobacterium tuberculosis response to environmental cues for the development of effective antitubercular drugs.PLoS biology · 2021Article
- Metabolomics reveals that the cAMP receptor protein regulates nitrogen and peptidoglycan synthesis inRSC advances · 2020Article
- Mycobacterial Control of Host Mitochondria: Bioenergetic and Metabolic Changes Shaping Cell Fate and Infection Outcome.Frontiers in cellular and infection microbiology · 2020Review
- AbmR (Rv1265) is a novel transcription factor of Mycobacterium tuberculosis that regulates host cell association and expression of the non-coding small RNA Mcr11.Molecular microbiology · 2018Article
- Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.Nature reviews. Microbiology · 2018Review
- Cyclic nucleotide signaling in Mycobacterium tuberculosis: an expanding repertoire.Pathogens and disease · 2018Article
- More than cholesterol catabolism: regulatory vulnerabilities in Mycobacterium tuberculosis.Current opinion in chemical biology · 2018Review
- Cholesterol and fatty acids grease the wheels of Mycobacterium tuberculosis pathogenesis.Pathogens and disease · 2018Review
- cAMP is an allosteric modulator of DNA-binding specificity in the cAMP receptor protein from Mycobacterium tuberculosis.The Journal of biological chemistryArticle
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) uses a complex 3', 5'-cyclic AMP (cAMP) signaling network to sense and respond to changing environments encountered during infection, so perturbation of cAMP signaling might be leveraged to disrupt Mtb pathogenesis. However, understanding of cAMP signaling pathways is hindered by the presence of at least 15 distinct adenylyl cyclases (ACs). Recently, the small molecule V-58 was shown to inhibit Mtb replication within macrophages and stimulate cAMP production in Mtb. Here we determined that V-58 rapidly and directly activates Mtb AC Rv1625c to produce high levels of cAMP regardless of the bacterial environment or growth medium. Metabolic inhibition by V-58 was carbon source dependent in Mtb and did not occur in Mycobacterium smegmatis, suggesting that V-58-mediated growth inhibition is due to interference with specific Mtb metabolic pathways rather than a generalized cAMP toxicity. Chemical stimulation of cAMP production by Mtb within macrophages also caused down regulation of TNF-α production by the macrophages, indicating a complex role for cAMP in Mtb pathogenesis. Together these studies describe a novel approach for targeted stimulation of cAMP production in Mtb, and provide new insights into the myriad roles of cAMP signaling in Mtb, particularly during Mtb's interactions with macrophages.
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Registered trials
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