ArticleInfection and immunity2012
The hydrophilic translocator for Vibrio parahaemolyticus, T3SS2, is also translocated.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Genomic insights into clinical non-O1/non-O139Microbiology spectrum · 2025Article
- Identification of a Family ofmSphere · 2021Article
- Adaptations ofFrontiers in microbiology · 2021Review
- Animal Models of Type III Secretion System-Mediated Pathogenesis.Pathogens (Basel, Switzerland) · 2019Review
- Vibrio variations on a type three theme.Current opinion in microbiology · 2019Review
- Genetic analysis of Vibrio parahaemolyticus intestinal colonization.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Type 3 Secretion System Island Encoded Proteins Required for Colonization by Non-O1/non-O139 SerogroupInfection and immunity · 2015Article
- Comparative RNA-Seq based dissection of the regulatory networks and environmental stimuli underlying Vibrio parahaemolyticus gene expression during infection.Nucleic acids research · 2014Article
- Remodeling of the intestinal brush border underlies adhesion and virulence of an enteric pathogen.mBio · 2014Article
- A Vibrio parahaemolyticus T3SS effector mediates pathogenesis by independently enabling intestinal colonization and inhibiting TAK1 activation.Cell reports · 2013Article
- The role of type III secretion system 2 in Vibrio parahaemolyticus pathogenicity.Journal of microbiology (Seoul, Korea) · 2012Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The pathogenesis of the diarrheal disease caused by Vibrio parahaemolyticus, a leading cause of seafood-associated enteritis worldwide, is dependent upon a type III secretion system, T3SS2. This apparatus enables the pathogen to inject bacterial proteins (effectors) into the cytosol of host cells and thereby modulate host processes. T3SS effector proteins transit into the host cell via a membrane pore (translocon) typically formed by 3 bacterial proteins. We have identified the third translocon protein for T3SS2: VopW, which was previously classified as an effector protein for a homologous T3SS in V. cholerae. VopW is a hydrophilic translocon protein; like other such proteins, it is not inserted into the host cell membrane but is required for insertion of the two hydrophobic translocators, VopB2 and VopD2, that constitute the membrane channel. VopW is not required for secretion of T3SS2 effectors into the bacterial culture medium; however, it is essential for transfer of these proteins into the host cell cytoplasm. Consequently, deletion of vopW abrogates the virulence of V. parahaemolyticus in several animal models of diarrheal disease. Unlike previously described hydrophilic translocators, VopW is itself translocated into the host cell cytoplasm, raising the possibility that it functions as both a translocator and an effector.
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