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Bacterial virulence factors targeting Rho GTPases: parasitism or symbiosis?
Abstract
In the past few years, an important question in microbiology has arisen from reports indicating that several pathogenic bacteria have evolved virulence factors directed towards a Ras subfamily of GTPases, namely the Rho GTPases. Progress made in studying both the virulence factors and the signaling pathways involving Rho GTPases has shed light on this crosstalk. One central question is raised by the findings that both activating and inactivating virulence factors that target Rho GTPases coexist in some pathogenic bacteria. Further studies on this peculiar aspect of the bacteria-host cell interactions, which leads to the outbreak of infectious diseases, might clarify whether this aspect of Rho GTPase activation or inactivation represents a finely adapted response of the pathogen for its own benefit or might lead to a reaction of the host against the bacteria.
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“This RAC2 Q61E protein modification within the G3/Switch II domain abolished the GTPase activity, thus confining the RAC GTPases into an active form (Boquet and Lemichez, 2003).”
From RAC2 gain-of-function variants causing inborn error of immunity drive NLRP3 inflammasome activation (2024) · cites this paper as Boquet and Lemichez, 2003
In the citing paper
“Mechanistically, the CNF1 induced a posttranslational modification consisting of the deamidation of glutamine 61 of RAC, converting this amino acid into a glutamate.”
From RAC2 gain-of-function variants causing inborn error of immunity drive NLRP3 inflammasome activation (2024) · cites this paper as Boquet and Lemichez, 2003
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Cited by
RAC2 gain-of-function variants causing inborn error of immunity drive NLRP3 inflammasome activation
Doye, A., Chaintreuil, P., Lagresle-Peyrou, C., Batistic, L., Marion, V., Munro, P., Loubatier, C., Chirara, R., Sorel, N., Bessot, B., et al. (2024) · Journal of Experimental Medicine · doi:10.1084/jem.20231562 · Cited by 12
Metadata
- Authors
- Boquet, P., & Lemichez, E.
- Venue
- Trends in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2003-05
- Volume
- 13
- Issue
- 5
- Pages
- 238-246
- ISSN
- 0962-8924
- Cited by
- 149
- References
- 2
- Language
- en
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