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Impact of host factors and invasive meningococci on bacterial adhesion, proliferation, primary nasal epithelial barrier function, and immune response

To investigate this hypothesis, we generated a truncated mutant comprising only the C-terminal region of ATG2A (amino acids 8471938) and lacking the amphipathic helix (ATG2A-CT-AH)

Beyond these classical PTMs, KHcy represents a pathological, nonenzymatic PTM that occurs in direct proportion to cellular Hcy and HTL concentrations and has emerged as a key mediator of protein dysfunction, cytotoxicity, inflammation, and atherothrombosis[15]

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