ArticleCellular microbiology2012
IQGAP1 mediates the disruption of adherens junctions to promote Escherichia coli K1 invasion of brain endothelial cells.
Article in Cellular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- The Pathological Activation of Microglia Is Modulated by Sexually Dimorphic Pathways.International journal of molecular sciences · 2023Review
- Hcp Proteins of the Type VI Secretion System Promote Avian PathogenicLife (Basel, Switzerland) · 2022Article
- Article
- Article
- Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption.Virulence · 2020Article
- The Post-amyloid Era in Alzheimer's Disease: Trust Your Gut Feeling.Frontiers in aging neuroscience · 2019Review
- CNS infection and immune privilege.Nature reviews. Neuroscience · 2018Review
- A journey into the brain: insight into how bacterial pathogens cross blood-brain barriers.Nature reviews. Microbiology · 2017Review
- IQGAP1 Mediates Hcp1-PromotedFrontiers in cellular and infection microbiology · 2017Article
- Article
- Escherichia coli K1 Modulates Peroxisome Proliferator-Activated Receptor γ and Glucose Transporter 1 at the Blood-Brain Barrier in Neonatal Meningitis.The Journal of infectious diseases · 2016Article
- Pertussis Toxin Exploits Specific Host Cell Signaling Pathways for Promoting Invasion and Translocation of Escherichia coli K1 RS218 in Human Brain-derived Microvascular Endothelial Cells.The Journal of biological chemistry · 2015Article
- IQGAP1 promotes CXCR4 chemokine receptor function and trafficking via EEA-1+ endosomes.The Journal of cell biology · 2015Article
- The biology of IQGAP proteins: beyond the cytoskeleton.EMBO reports · 2015Review
- Serotype O18 avian pathogenic and neonatal meningitis Escherichia coli strains employ similar pathogenic strategies for the onset of meningitis.Virulence · 2015Article
- Pathogens penetrating the central nervous system: infection pathways and the cellular and molecular mechanisms of invasion.Clinical microbiology reviews · 2014Review
- Intracellular Haemophilus influenzae invades the brain: is zyxin a critical blood brain barrier component regulated by TNF-α?Virulence · 2014Article
- Identification of minimum carbohydrate moiety in N-glycosylation sites of brain endothelial cell glycoprotein 96 for interaction with Escherichia coli K1 outer membrane protein A.Microbes and infection · 2014Article
- Angiotensin II receptor type 1--a novel target for preventing neonatal meningitis in mice by Escherichia coli K1.The Journal of infectious diseases · 2014Article
- Rac1 is deactivated at integrin activation sites through an IQGAP1-filamin-A-RacGAP1 pathway.Journal of cell science · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The transcellular entry of Escherichia coli K1 through human brain microvascular endothelial cells (HBMEC) is responsible for tight junction disruption, leading to brain oedema in neonatal meningitis. Previous studies demonstrated that outer membrane protein A (OmpA) of E. coli K1 interacts with its receptor, Ecgp96, to induce PKC-α phosphorylation, adherens junction (AJ) disassembly (by dislodging β-catenin from VE-cadherin), and remodelling of actin in HBMEC. We report here that IQGAP1 mediates β-catenin dissociation from AJs to promote actin polymerization required for E. coli K1 invasion of HBMEC. Overexpression of C-terminal truncated IQGAP1 (IQΔC) that cannot bind β-catenin prevents both AJ disruption and E. coli K1 entry. Of note, phospho-PKC-α interacts with the C-terminal portion of Ecgp96 as well as with VE-cadherin after IQGAP1-mediated AJ disassembly. HBMEC overexpressing either C-terminal truncated Ecgp96 (Ecgp96Δ200) or IQΔC upon infection with E. coli showed no interaction of phospho-PKC-α with Ecgp96. These data indicate that the binding of OmpA to Ecgp96 induces PKC-α phosphorylation and association of phospho-PKC-α with Ecgp96, and then signals IQGAP1 to detach β-catenin from AJs. Subsequently, IQGAP1/β-catenin bound actin translocates to the site of E. coli K1 attachment to promote invasion.
Indexed as
Identifiers
What OpenQuestion holds
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.