ArticleThe Journal of biological chemistry2010
Bordetella adenylate cyclase toxin promotes calcium entry into both CD11b+ and CD11b- cells through cAMP-dependent L-type-like calcium channels.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Article
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- Functional and structural consequences of epithelial cell invasion by Bordetella pertussis adenylate cyclase toxin.PloS one · 2020Article
- Review
- Phospholipase A activity of adenylate cyclase toxin mediates translocation of its adenylate cyclase domain.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Bordetella adenylate cyclase toxin interacts with filamentous haemagglutinin to inhibit biofilm formation in vitro.Molecular microbiology · 2017Article
- Design and Synthesis of Fluorescent Acyclic Nucleoside Phosphonates as Potent Inhibitors of Bacterial Adenylate Cyclases.ChemMedChem · 2016Article
- Adenylate Cyclase Toxin promotes bacterial internalisation into non phagocytic cells.Scientific reports · 2015Article
- Amidate prodrugs of 9-[2-(phosphonomethoxy)ethyl]adenine as inhibitors of adenylate cyclase toxin from Bordetella pertussis.Antimicrobial agents and chemotherapy · 2014Article
- Quantification of the adenylate cyclase toxin of Bordetella pertussis in vitro and during respiratory infection.Infection and immunity · 2013Article
- Article
- Calpain-Mediated Processing of Adenylate Cyclase Toxin Generates a Cytosolic Soluble Catalytically Active N-Terminal Domain.PloS one · 2013Article
- Role of CD11b/CD18 in the process of intoxication by the adenylate cyclase toxin of Bordetella pertussis.Infection and immunity · 2012Article
- The Bordetella pertussis adenylate cyclase toxin binds to T cells via LFA-1 and induces its disengagement from the immune synapse.The Journal of experimental medicine · 2011Article
- Adenylate cyclase toxin promotes internalisation of integrins and raft components and decreases macrophage adhesion capacity.PloS one · 2011Article
- Modulation of the host interferon response and ISGylation pathway by B. pertussis filamentous hemagglutinin.PloS one · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenylate cyclase toxin (ACT), a 200 kDa protein, is an essential virulence factor for Bordetella pertussis, the bacterium that causes whooping cough. ACT is a member of the pore-forming RTX (repeats-in-toxin) family of proteins that share a characteristic calcium-binding motif of Gly- and Asp-rich nonapeptide repeats and a marked cytolytic or cytotoxic activity. In addition, ACT exhibits a distinctive feature: it has an N-terminal calmodulin-dependent adenylate cyclase domain. Translocation of this domain into the host cytoplasm results in uncontrolled production of cAMP, and it has classically been assumed that this surge in cAMP is the basis for the toxin-mediated killing. Several members of the RTX family of toxins, including ACT, have been shown to induce intracellular calcium increases, through different mechanisms. We show here that ACT stimulates a raft-mediated calcium influx, through its cAMP production activity, that activates PKA, which in turn activates calcium channels with L-type properties. This process is shown to occur both in CD11b(+) and CD11b(-) cells, suggesting a common mechanism, independent of the toxin receptor. We also show that this ACT-induced calcium influx does not correlate with the toxin-induced cytotoxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.