meningococcal infections/tyrosine

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Significance of the changes in plasma amino-acid levels in meningococcal infection.

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A series of patients with meningococcal infections have been studied and divided in two groups: Group I patients with meningococcal sepsis and group II, those with meningococcal meningitis. Patients in group I presented with more severe encephalopathy, shock, DIC and acute systemic complications.

Molecular characterization of properdin deficiency type III: dysfunction produced by a single point mutation in exon 9 of the structural gene causing a tyrosine to aspartic acid interchange.

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Inherited properdin deficiency is an X-linked recessive disorder clinically manifested by susceptibility to meningococcal disease. Deficiency of properdin is characterized by complete absence (type I), very low level presence (type II), or the presence of a dysfunctional properdin protein in serum

Prevalence of mutations leading to complete C6 deficiency (C6Q0) in the Western Cape, South Africa and detection of novel mutations leading to C6Q0 in an Irish family.

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Complement component C6 is one of five terminal complement components incorporated into the membrane attack complex. Complete deficiency of C6 (C6Q0) leads to an increased susceptibility to Neisseria meningitidis infections, and affected individuals typically present with recurrent meningococcal

Two mutations of the C7 gene, c.1424G > A and c.281-1G > T, in two Korean families.

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Complement C7 deficiency is associated with increased susceptibility to meningococcal infection. The genetic alterations of C7 deficiency are known to be sporadic and heterogeneous worldwide. We investigated molecular basis of C7 deficiency in two unrelated Korean families, in which the index cases

Role of epidermal growth factor receptor signaling in the interaction of Neisseria meningitidis with endothelial cells.

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Neisseria meningitidis, the causative agent of meningitis and septicemia, attaches to and invades various cell types. Both steps induce and/or require tyrosine phosphorylation of host cell proteins. Here, we used a phospho array platform to identify active receptor tyrosine kinases (RTKs) and key

Meningococcus Hijacks a β2-adrenoceptor/β-Arrestin pathway to cross brain microvasculature endothelium.

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Following pilus-mediated adhesion to human brain endothelial cells, meningococcus (N. meningitidis), the bacterium causing cerebrospinal meningitis, initiates signaling cascades, which eventually result in the opening of intercellular junctions, allowing meningeal colonization. The signaling

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