(Q37456615)

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Contribution of interactions between complement inhibitor C4b-binding protein and pathogens to their ability to establish infection with particular emphasis on Neisseria gonorrhoeae.

scientific article published on December 2008

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26 January 2020

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Europe PubMed Central

Contribution of interactions between complement inhibitor C4b-binding protein and pathogens to their ability to establish infection with particular emphasis on Neisseria gonorrhoeae (English)

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Europe PubMed Central

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:19388165%20AND%20SRC:MED&resulttype=core&format=json

26 January 2020

Neisseria gonorrhoeae

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26 January 2020

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Sanjay Ram

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26 January 2020

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1 December 2008

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26 January 2020

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26 January 2020

26 Suppl 8

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26 January 2020

I49-55

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:19388165%20AND%20SRC:MED&resulttype=core&format=json

26 January 2020

Complement deficiency and disease

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Investigations on the cell type responsible for the endometrial secretion of complement component 3 (C3)

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Complement Processing and Immunoglobulin Binding toNeisseria gonorrhoeaeDetermined In Vitro Simulates In Vivo Effects

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Modulation of the classical pathway C3 convertase by plasma proteins C4 binding protein and C3b inactivator

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CCP1-4 of the C4b-binding protein alpha-chain are required for factor I mediated cleavage of complement factor C3b.

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Structural requirements for the intracellular subunit polymerization of the complement inhibitor C4b-binding protein

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Structure and flexibility of the multiple domain proteins that regulate complement activation

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A novel non-synonymous polymorphism (p.Arg240His) in C4b-binding protein is associated with atypical hemolytic uremic syndrome and leads to impaired alternative pathway cofactor activity

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Protein S binding in relation to the subunit composition of human C4b-binding protein

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Extreme sequence divergence but conserved ligand-binding specificity in Streptococcus pyogenes M protein

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Human C4b-binding protein has overlapping, but not identical, binding sites for C4b and streptococcal M proteins

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Human C4b-binding protein, structural basis for interaction with streptococcal M protein, a major bacterial virulence factor

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Streptococcal M protein: structural studies of the hypervariable region, free and bound to human C4BP.

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Binding properties of protein Arp, a bacterial IgA-receptor

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Isolated hypervariable regions derived from streptococcal M proteins specifically bind human C4b-binding protein: implications for antigenic variation

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Evasion of phagocytosis through cooperation between two ligand-binding regions in Streptococcus pyogenes M protein.

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A novel interaction of outer membrane protein A with C4b binding protein mediates serum resistance of Escherichia coli K1.

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The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat

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Logarithmic phase Escherichia coli K1 efficiently avoids serum killing by promoting C4bp-mediated C3b and C4b degradation

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Bordetella pertussis binds to human C4b-binding protein (C4BP) at a site similar to that used by the natural ligand C4b

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Impact of the changing epidemiology of fungal infections in the 1990s

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Opportunistic candidiasis: an epidemic of the 1980s.

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The yeast Candida albicans binds complement regulators factor H and FHL-1.

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The hyphal and yeast forms of Candida albicans bind the complement regulator C4b-binding protein

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Immune evasion by acquisition of complement inhibitors: the mould Aspergillus binds both factor H and C4b binding protein

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The emerging pathogen Moraxella catarrhalis interacts with complement inhibitor C4b binding protein through ubiquitous surface proteins A1 and A2.

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Interaction with C4b-binding protein contributes to nontypeable Haemophilus influenzae serum resistance

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Relapsing fever spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H

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The complement regulator factor H binds to the surface protein OspE of Borrelia burgdorferi

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Immune evasion of Borrelia burgdorferi by acquisition of human complement regulators FHL-1/reconectin and Factor H

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Binding of the complement inhibitor C4bp to serogroup B Neisseria meningitidis

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Gonococci in Urethral Exudates possess a Virulence Factor lost on Subculture

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Cytidine 5'-monophospho-N-acetyl neuraminic acid and a low molecular weight factor from human blood cells induce lipopolysaccharide alteration in gonococci when conferring resistance to killing by human serum

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A novel sialic acid binding site on factor H mediates serum resistance of sialylated Neisseria gonorrhoeae

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Modification by Sialic Acid of Neisseria gonorrhoeae Lipooligosaccharide Epitope Expression in Human Urethral Exudates: An Immunoelectron Microscopic Analysis

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10.1016/J.VACCINE.2008.11.049

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Europe PubMed Central

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:19388165%20AND%20SRC:MED&resulttype=core&format=json

26 January 2020

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:19388165%20AND%20SRC:MED&resulttype=core&format=json

26 January 2020

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