Binding of factor H to tubular epithelial cells limits interstitial complement activation in ischemic injury - Wikidata - awgldk - TriplyDB

Binding of factor H to tubular epithelial cells limits interstitial complement activation in ischemic injury

Binding of factor H to tubular epithelial cells limits interstitial complement activation in ischemic injury

http://www.wikidata.org/entity/Q35097512

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Properdin: a tightly regulated critical inflammatory modulator Properdin has an ascendancy over factor H regulation in complement-mediated renal tubular damage.Antepartum or immediate postpartum renal biopsies in preeclampsia/eclampsia of pregnancy: new morphologic and clinical findings Tissue-specific deletion of Crry from mouse proximal tubular epithelial cells increases susceptibility to renal ischemia-reperfusion injury.Factor h and properdin recognize different epitopes on renal tubular epithelial heparan sulfate.Defective complement inhibitory function predisposes to renal disease.Renoprotective Mechanism of Remote Ischemic Preconditioning Based on Transcriptomic Analysis in a Porcine Renal Ischemia Reperfusion Injury Model.Mouse model of ischemic acute kidney injury: technical notes and tricks Taming lupus-a new understanding of pathogenesis is leading to clinical advances.Essential role of surface-bound complement factor H in controlling immune complex-induced arthritis Detection of complement activation using monoclonal antibodies against C3d.Properdin-Mediated C5a Production Enhances Stable Binding of Platelets to Granulocytes in Human Whole Blood.Identification of a novel mode of complement activation on stimulated platelets mediated by properdin and C3(H2O).Interaction of uromodulin and complement factor H enhances C3b inactivation.The role of the complement system in acute kidney injury.Complement as a multifaceted modulator of kidney transplant injury.The bittersweet taste of tubulo-interstitial glycans.Efficacy of Targeted Complement Inhibition in Experimental C3 Glomerulopathy.Which pathways trigger the role of complement in ischaemia/reperfusion injury?The Murine Factor H-Related Protein FHR-B Promotes Complement Activation Modulation of the Alternative Pathway of Complement by Murine Factor H-Related Proteins.Intracellular Activation of Complement 3 Is Responsible for Intestinal Tissue Damage during Mesenteric Ischemia.Complement factor H protects mice from ischemic acute kidney injury but is not critical for controlling complement activation by glomerular IgM.Targeting Complement Pathways During Cold Ischemia and Reperfusion Prevents Delayed Graft Function.

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Binding of factor H to tubular epithelial cells limits interstitial complement activation in ischemic injury

http://www.wikidata.org/entity/Q35097512

description

2011 nî lūn-bûn

@nan

2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի մայիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Binding of factor H to tubular ...... activation in ischemic injury

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Binding of factor H to tubular ...... activation in ischemic injury

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type

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Binding of factor H to tubular ...... activation in ischemic injury

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Binding of factor H to tubular ...... activation in ischemic injury

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Binding of factor H to tubular ...... activation in ischemic injury

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Binding of factor H to tubular ...... activation in ischemic injury

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Kidney International

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Binding of factor H to tubular ...... activation in ischemic injury

@en

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Amanda Holland-Neidermyer

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Brandon Renner

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Danica Ljubanovic

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Derek Strassheim

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Joshua M Thurman

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Michael K Pangburn

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Ryan Goldberg

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Stephen Tomlinson

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V Michael Holers

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P2860

Factor I is required for the development of membranoproliferative glomerulonephritis in factor H-deficient mice

Molecular organization and function of the complement system

The simple design of complement factor H: Looks can be deceiving.

Spontaneous hemolytic uremic syndrome triggered by complement factor H lacking surface recognition domains.

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

Targeted complement inhibition by C3d recognition ameliorates tissue injury without apparent increase in susceptibility to infection.

Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischemia/reperfusion.

Complement receptor 2-mediated targeting of complement inhibitors to sites of complement activation.

Alternative complement pathway in the pathogenesis of disease mediated by anti-neutrophil cytoplasmic autoantibodies

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

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165-173

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scholarly article

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10.1038/KI.2011.115

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2

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Viviana Ferreira

Matthew C Pickering

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2011-05-04T00:00:00Z

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51099738

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