Complement activity is regulated in C3 glomerulopathy by IgG–factor H fusion proteins with and without properdin targeting domains - ScienceDirect

Complement activity is regulated in C3 glomerulopathy by IgG–factor H fusion proteins with and without properdin targeting domains - ScienceDirect

A synthetic protein as efficient multitarget regulator against complement over-activation

Biomolecules, Free Full-Text

C3 Glomerulopathy: Update on Pathogenesis and Treatment in: Kidney News Volume 13 Issue 4 (2021)

Frontiers CFH and CFHR Copy Number Variations in C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis

Antibody recognition of complement factor H reveals a flexible loop involved in atypical hemolytic uremic syndrome pathogenesis - Journal of Biological Chemistry

C3d-Targeted factor H inhibits tissue complement in disease models and reduces glomerular injury without affecting circulating complement - ScienceDirect

A C3-specific nanobody that blocks all three activation pathways in the human and murine complement system - ScienceDirect

Complement-mediated kidney diseases - ScienceDirect

Frontiers Complement Factor H-Related Proteins FHR1 and FHR5 Interact With Extracellular Matrix Ligands, Reduce Factor H Regulatory Activity and Enhance Complement Activation

Glomerular Disease of Complement Dysregulation (C3 Glomerulopathy, Atypical Hemolytic-Uremic Syndrome)

PDF) Properdin Can Initiate Complement Activation by Binding Specific Target Surfaces and Providing a Platform for De Novo Convertase Assembly

Glomerular Complement Factor H–Related Protein 5 (FHR5) Is Highly Prevalent in C3 Glomerulopathy and Associated With Renal Impairment - ScienceDirect