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• W1568251135 startingPage "925" @default.
• W1568251135 abstract "Neisseria meningitidis is a human pathogen that can cause fatal sepsis and meningitis once it reaches the blood stream and the nervous system. Here we demonstrate that a fragment, released upon proteolysis of the surface-exposed protein Neisserial Heparin Binding Antigen (NHBA), by the bacterial protease NalP, alters the endothelial permeability by inducing the internalization of the adherens junction protein VE-cadherin. We found that C2 rapidly accumulates in mitochondria where it induces the production of reactive oxygen species: the latter are required for the phosphorylation of the junctional protein and for its internalization that, in turn, is responsible for the endothelial leakage. Our data support the notion that the NHBA-derived fragment C2 might contribute to the extensive vascular leakage typically associated with meningococcal sepsis." @default.
• W1568251135 created "2016-06-24" @default.
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• W1568251135 date "2014-01-08" @default.
• W1568251135 modified "2023-10-14" @default.
• W1568251135 title "The C2 fragment from<i>N</i><i>eisseria meningitidis</i>antigen NHBA increases endothelial permeability by destabilizing adherens junctions" @default.
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• W1568251135 doi "https://doi.org/10.1111/cmi.12250" @default.
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