Properdin: a tightly regulated critical inflammatory modulator - Wikidata - wikimedia - TriplyDB

Properdin: a tightly regulated critical inflammatory modulator

Properdin: a tightly regulated critical inflammatory modulator

http://www.wikidata.org/entity/Q28069187

about

Complement factor P is a ligand for the natural killer cell-activating receptor NKp46.Properdin binding to complement activating surfaces depends on initial C3b deposition.Complement component C3 - The "Swiss Army Knife" of innate immunity and host defense Complement factor P: promoting the antibacterial activity of natural killer cells.Functional and structural insight into properdin control of complement alternative pathway amplification.Extracellular vesicles from KSHV-infected endothelial cells activate the complement system.The renaissance of complement therapeutics.Preformed mediators of defense-Gatekeepers enter the spotlight.Advances in our Understanding of the Pathogenesis of Hemolytic Uremic Syndromes.Retinal Basal Laminar Deposits in Complement fH/fP Mouse Model of Dense Deposit Disease.Be on Target: Strategies of Targeting Alternative and Lectin Pathway Components in Complement-Mediated Diseases

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P2860

Properdin: a tightly regulated critical inflammatory modulator

http://www.wikidata.org/entity/Q28069187

description

2016 nî lūn-bûn

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2016 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2016 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2016年の論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年论文

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name

Properdin: a tightly regulated critical inflammatory modulator

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Properdin: a tightly regulated critical inflammatory modulator

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Properdin: a tightly regulated critical inflammatory modulator

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Properdin: a tightly regulated critical inflammatory modulator

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Properdin: a tightly regulated critical inflammatory modulator

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Properdin: a tightly regulated critical inflammatory modulator

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Adam Z. Blatt

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Sabina Pathan

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Viviana P. Ferreira

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Creative Commons Attribution

P2860

Cathepsin G activates protease-activated receptor-4 in human platelets

Bivalent and co-operative binding of complement factor H to heparan sulfate and heparin

Analysis of the interaction between properdin and factor B, components of the alternative-pathway C3 convertase of complement

Structure of complement factor H carboxyl-terminus reveals molecular basis of atypical haemolytic uremic syndrome.

Control of the amplification convertase of complement by the plasma protein beta1H

Design and development of TT30, a novel C3d-targeted C3/C5 convertase inhibitor for treatment of human complement alternative pathway-mediated diseases

The junctional adhesion molecule 3 (JAM-3) on human platelets is a counterreceptor for the leukocyte integrin Mac-1

Human complement C3b inactivator: isolation, characterization, and demonstration of an absolute requirement for the serum protein beta1H for cleavage of C3b and C4b in solution

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

Clopidogrel inhibits platelet-leukocyte interactions and thrombin receptor agonist peptide-induced platelet activation in patients with an acute coronary syndrome

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172-190

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10.1111/IMR.12466

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