ArticleProceedings of the National Academy of Sciences of the United States of America2001
Overexpression of the inositol phosphatase SopB in human 293 cells stimulates cellular chloride influx and inhibits nuclear mRNA export.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 94 citations in OpenAlex.
- Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression.Nature communications · 2026Article
- Enzymatic versatility of the salmonella effector SopB enables manipulation of host phosphoinositide signalling.Discover bacteria · 2026Review
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Virulence and Antimicrobial-Resistant Gene Profiles ofInternational journal of microbiology · 2024Article
- Kinase-independent synthesis of 3-phosphorylated phosphoinositides by a phosphotransferase.Nature cell biology · 2022Article
- Aiding and abetting cancer: mRNA export and the nuclear pore.Trends in cell biology · 2013Review
- Salmonella type III effector SopB modulates host cell exocytosis.Emerging microbes & infections · 2013Article
- The actin-polymerizing activity of SipA is not essential for Salmonella enterica serovar Typhimurium-induced mucosal inflammation.Infection and immunity · 2013Article
- Interplay between the QseC and QseE bacterial adrenergic sensor kinases in Salmonella enterica serovar Typhimurium pathogenesis.Infection and immunity · 2012Article
- MHO1, an evolutionarily conserved gene, is synthetic lethal with PLC1; Mho1p has a role in invasive growth.PloS one · 2012Article
- Control of mRNA export and translation termination by inositol hexakisphosphate requires specific interaction with Gle1.The Journal of biological chemistry · 2010Article
- Expression of inositol 1,3,4-trisphosphate 5/6-kinase (ITPK1) and its role in neural tube defects.Advances in enzyme regulation · 2010Article
- Neural tube defects in mice with reduced levels of inositol 1,3,4-trisphosphate 5/6-kinase.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Dual functions for the Schizosaccharomyces pombe inositol kinase Ipk1 in nuclear mRNA export and polarized cell growth.Eukaryotic cell · 2009Article
- Review
- Alteration of epithelial structure and function associated with PtdIns(4,5)P2 degradation by a bacterial phosphatase.The Journal of general physiology · 2007Article
- Roles for inositol polyphosphate kinases in the regulation of nuclear processes and developmental biology.Advances in enzyme regulation · 2007Review
- Intestinal innate immunity and the pathogenesis of Salmonella enteritis.Immunologic research · 2007Article
- Pathogenicity of Salmonella: SopE-mediated membrane ruffling is independent of inositol phosphate signals.FEBS letters · 2006Article
- Escherichia coli heat stable (STa) enterotoxin and the upper small intestine: lack of evidence in vivo for net fluid secretion.The Journal of membrane biology · 2005Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
SopB is an inositol phosphate phosphatase that is a virulence factor in Salmonella species. We have overexpressed SopB cDNA in a tetracycline-dependent system in human embryonic 293 cells, and used this model system to directly analyze the role of SopB in altering inositol metabolite levels in vivo. Addition of tetracycline to these cells resulted in the rapid induction of SopB expression, which was coincident with perturbations in the cellular levels of multiple soluble inositol phosphates. All of the changes induced by SopB expression were reversed within 24 h on removal of tetracycline from media. Specifically, cellular inositol 1,3,4,5,6-pentakisphosphate (InsP(5)) and inositol hexakisphosphate (InsP(6)) levels were depleted within 4 to 6 h after inducing SopB expression. A transient rise in cellular inositol 1,4,5,6-tetrakisphosphate was also observed and was accompanied by increased chloride channel activity. This indicates that SopB alone is sufficient for changes in chloride channel function in cells infected with Salmonella organisms. Depletion of inositol phosphates, including InsP(5) and InsP(6) metabolites, was coincident with the accumulation of polyadenylated RNA in the nucleus. This suggested that a defect in nuclear export had occurred. Moreover, the penetrance of the export defect required localization of SopB to the nucleus. These results provide evidence that inositol phosphate productions may be required for efficient mRNA export in mammalian cells.
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