Structural basis for sialic acid-mediated self-recognition by complement factor H (Q27696183)

6

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Jonathan P Hannan

object named as

Jonathan P Hannan

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David Kavanagh

object named as

David Kavanagh

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author name string

Bärbel S Blaum

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Andrew P Herbert

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Dušan Uhrín

Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy

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publication date

January 2015

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published in

Nature Chemical Biology

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volume

11

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page(s)

77-82

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issue

1

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cites work

1 reference

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The central portion of factor H (modules 10-15) is compact and contains a structurally deviant CCP module

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Structure of C3b reveals conformational changes that underlie complement activity

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Structural basis for complement factor H linked age-related macular degeneration

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Siglecs as sensors of self in innate and adaptive immune responses

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Structural basis for engagement by complement factor H of C3b on a self surface

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Dual interaction of factor H with C3d and glycosaminoglycans in host-nonhost discrimination by complement

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Disease-associated sequence variations congregate in a polyanion recognition patch on human factor H revealed in three-dimensional structure

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Structural and functional characterization of the product of disease-related factor H gene conversion

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Mutations in alternative pathway complement proteins in American patients with atypical hemolytic uremic syndrome

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Mutation in the key enzyme of sialic acid biosynthesis causes severe glomerular proteinuria and is rescued by N-acetylmannosamine

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Structural Basis for Complement Evasion by Lyme Disease Pathogen Borrelia burgdorferi

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Complement factor H related proteins (CFHRs)

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Structural implications of Siglec-5-mediated sialoglycan recognition

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The Cell Adhesion Molecule “CAR” and Sialic Acid on Human Erythrocytes Influence Adenovirus In Vivo Biodistribution

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Integration, scaling, space-group assignment and post-refinement

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Refinement of macromolecular structures by the maximum-likelihood method

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Complement: a key system for immune surveillance and homeostasis

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The relevance of complement to virus biology

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Membrane complement regulatory proteins

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Complement evasion by human pathogens

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Factor H mediated cell surface protection from complement is critical for the survival of PNH erythrocytes.

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The complement inhibitors Crry and factor H are critical for preventing autologous complement activation on renal tubular epithelial cells.

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Regulation by membrane sialic acid of β1H-dependent decay-dissociation of amplification C3 convertase of the alternative complement pathway

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Complement C3 convertase: Cell surface restriction of β1H control and generation of restriction on neuraminidase-treated cells

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

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Discrimination between host and pathogens by the complement system.

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Impaired binding of the age-related macular degeneration-associated complement factor H 402H allotype to Bruch's membrane in human retina.

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Tissue-specific host recognition by complement factor H is mediated by differential activities of its glycosaminoglycan-binding regions

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Dendritic cells: a spot on sialic Acid.

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Discrimination between activators and nonactivators of the alternative pathway of complement: regulation via a sialic acid/polyanion binding site on factor H

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Group epitope mapping by saturation transfer difference NMR to identify segments of a ligand in direct contact with a protein receptor

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Direct observation of ligand binding to membrane proteins in living cells by a saturation transfer double difference (STDD) NMR spectroscopy method shows a significantly higher affinity of integrin alpha(IIb)beta3 in native platelets than in liposom

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Atypical hemolytic uremic syndrome

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Properdin can initiate complement activation by binding specific target surfaces and providing a platform for de novo convertase assembly

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An autosomal dominant gene regulates the extent of 9-O-acetylation of murine erythrocyte sialic acids. A probable explanation for the variation in capacity to activate the human alternate complement pathway

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The binding of factor H to a complex of physiological polyanions and C3b on cells is impaired in atypical hemolytic uremic syndrome.

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Rational engineering of a minimized immune inhibitor with unique triple-targeting properties

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A Siglec-like sialic-acid-binding motif revealed in an adenovirus capsid protein

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Inhibition of the alternative pathway of human complement by structural analogues of sialic acid

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12 December 2020

Critical role of the C-terminal domains of factor H in regulating complement activation at cell surfaces

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Regulation of alternative pathway complement activation by glycosaminoglycans: specificity of the polyanion binding site on factor H

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Identifiers

DOI

10.1038/NCHEMBIO.1696

1 reference

Consolidated OpenCitations Corpus – April 2017

Dimensions Publication ID

2104835

1043983949

0 references

2104835

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference