ArticlePathogens and disease2016
Intracellular disassembly and activity of pertussis toxin require interaction with ATP.
Article in Pathogens and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- ER-transiting bacterial toxins amplify STING innate immune responses and elicit ER stress.Infection and immunity · 2024Article
- The Chaperonin TRiC/CCT Inhibitor HSF1A Protects Cells from Intoxication with Pertussis Toxin.Toxins · 2024Article
- Reduction is sufficient for the disassembly of ricin and Shiga toxin 1 but notInfection and immunity · 2023Article
- Domperidone InhibitsToxins · 2023Article
- Inhibition of Pertussis Toxin by Human α-Defensins-1 and -5: Differential Mechanisms of Action.International journal of molecular sciences · 2023Article
- Crystal structures of pertussis toxin with NADThe Journal of biological chemistry · 2022Article
- Novel Strategies to Inhibit Pertussis Toxin.Toxins · 2022Review
- Cellular Activity ofToxins · 2021Article
- Article
- Pharmacological targeting of host chaperones protects from pertussis toxin in vitro and in vivo.Scientific reports · 2021Article
- Review
- Role of Major Toxin Virulence Factors in Pertussis Infection and Disease Pathogenesis.Advances in experimental medicine and biology · 2019Article
- Humanised monoclonal antibodies neutralise pertussis toxin by receptor blockade and reduced retrograde trafficking.Cellular microbiology · 2018Article
- Article
- Thermal Unfolding of the Pertussis Toxin S1 Subunit Facilitates Toxin Translocation to the Cytosol by the Mechanism of Endoplasmic Reticulum-Associated Degradation.Infection and immunity · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The active subunit (S1) of pertussis toxin (PT), a major virulence factor of Bordetella pertussis, ADP-ribosylates Gi proteins in the mammalian cell cytosol to inhibit GPCR signaling. The intracellular pathway of PT includes endocytosis and retrograde transport to the trans-Golgi network (TGN) and endoplasmic reticulum (ER). Subsequent translocation of S1 to the cytosol is presumably preceded by dissociation from the holotoxin. In vitro, such dissociation is stimulated by interaction of PT with ATP. To investigate the role of this interaction in cellular events, we engineered a form of PT (PTDM) with changes to two amino acids involved in the interaction with ATP. PTDM was reduced in (1) binding to ATP, (2) dissociability by interaction with ATP, (3) in vitro enzymatic activity and (4) cellular ADP-ribosylation activity. In cells treated with PTDM carrying target sequences for organelle-specific modifications, normal transport to the TGN and ER occurred, but N-glycosylation patterns of the S1 and S4 subunits were consistent with an inability of PTDM to dissociate in the ER. These results indicate a requirement for interaction with ATP for PT dissociation in the ER and cellular activity. They also indicate that the retrograde transport route is the cellular intoxication pathway for PT.
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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.