ArticleProceedings of the National Academy of Sciences of the United States of America1997
D-myo-Inositol 1,4,5,6-tetrakisphosphate produced in human intestinal epithelial cells in response to Salmonella invasion inhibits phosphoinositide 3-kinase signaling pathways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 100 citations in OpenAlex.
- 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
- Simultaneous HPLC determination of soluble signaling molecules and metabolic status in neuroblastoma cell cultures.Physiological reports · 2025Article
- Functions, Mechanisms, and therapeutic applications of the inositol pyrophosphates 5PP-InsPJournal of cardiovascular translational research · 2024Review
- Multiple Inositol Polyphosphate Phosphatase Compartmentalization Separates Inositol Phosphate Metabolism from Inositol Lipid Signaling.Biomolecules · 2023Article
- Pathophysiology of avian intestinal ion transport.World's poultry science journal · 2018Article
- Broad Spectrum Anticancer Activity of Myo-Inositol and Inositol Hexakisphosphate.International journal of endocrinology · 2016Review
- Defining signal transduction by inositol phosphates.Sub-cellular biochemistry · 2012Review
- Article
- Construction of recombinant attenuated Salmonella enterica serovar typhimurium vaccine vector strains for safety in newborn and infant mice.Clinical and vaccine immunology : CVI · 2010Article
- Media ion composition controls regulatory and virulence response of Salmonella in spaceflight.PloS one · 2008Article
- Allergen-IgE complexes trigger CD23-dependent CCL20 release from human intestinal epithelial cells.Gastroenterology · 2007Article
- Inositol 1,3,4,5-tetrakisphosphate negatively regulates phosphatidylinositol-3,4,5- trisphosphate signaling in neutrophils.Immunity · 2007Article
- Alteration of epithelial structure and function associated with PtdIns(4,5)P2 degradation by a bacterial phosphatase.The Journal of general physiology · 2007Article
- Pathogenicity of Salmonella: SopE-mediated membrane ruffling is independent of inositol phosphate signals.FEBS letters · 2006Article
- Inositol polyphosphate derivative inhibits Na+ transport and improves fluid dynamics in cystic fibrosis airway epithelia.American journal of physiology. Cell physiology · 2005Article
- Cooperative interactions between flagellin and SopE2 in the epithelial interleukin-8 response to Salmonella enterica serovar typhimurium infection.Infection and immunity · 2004Article
- Modulation and utilization of host cell phosphoinositides by Salmonella spp.Infection and immunity · 2004Review
- Conversion of PtdIns(4,5)P(2) into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology.The EMBO journal · 2002Article
- Diverse virulence traits underlying different clinical outcomes of Salmonella infection.The Journal of clinical investigation · 2001Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several inositol-containing compounds play key roles in receptor-mediated cell signaling events. Here, we describe a function for a specific inositol polyphosphate, D-myo-inositol 1,4,5,6-tetrakisphosphate [Ins(1,4,5,6)P4], that is produced acutely in response to a receptor-independent process. Thus, infection of intestinal epithelial cells with the enteric pathogen Salmonella, but not with other invasive bacteria, induced a multifold increase in Ins(1,4,5,6)P4 levels. To define a specific function of Ins(1,4,5,6)P4, a membrane-permeant, hydrolyzable ester was used to deliver it to the intracellular compartment, where it antagonized epidermal growth factor (EGF)-induced inhibition of calcium-mediated chloride (Cl-) secretion (CaMCS) in intestinal epithelia. This EGF function is likely mediated through a phosphoinositide 3-kinase (PtdIns3K)-dependent mechanism because the EGF effects are abolished by wortmannin, and three different membrane-permeant esters of the PtdIns3K product phosphatidylinositol 3,4,5-trisphosphate mimicked the EGF effect on CaMCS. We further demonstrate that Ins(1,4,5,6)P4 antagonized EGF signaling downstream of PtdIns3K because Ins(1,4,5, 6)P4 interfered with the PtdInsP3 effect on CaMCS without affecting PtdIns3K activity. Thus, elevation of Ins(1,4,5,6)P4 in Salmonella-infected epithelia may promote Cl- flux by antagonizing EGF inhibition mediated through PtdIns3K and PtdInsP3.
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