Results 21 to 30 of about 3,146 (147)

Properdin Is a Key Player in Lysis of Red Blood Cells and Complement Activation on Endothelial Cells in Hemolytic Anemias Caused by Complement Dysregulation

open access: yesFrontiers in Immunology, 2020
The complement system alternative pathway (AP) can be activated excessively in inflammatory diseases, particularly when there is defective complement regulation.
Jin Y. Chen   +8 more
doaj   +1 more source

Nephritic Factors: An Overview of Classification, Diagnostic Tools and Clinical Associations

open access: yesFrontiers in Immunology, 2019
Nephritic factors comprise a heterogeneous group of autoantibodies against neoepitopes generated in the C3 and C5 convertases of the complement system, causing its dysregulation.
Fernando Corvillo   +11 more
doaj   +1 more source

Ultrastructure of cobra venom factor-dependent C3/C5 convertase and its zymogen, factor B of human complement.

open access: yesJournal of Biological Chemistry, 1982
The molecular architecture of the cobra venom factor (CVF)-dependent C3/C5 convertase (EC 3.4.21.47) of human complement was deduced from electron microscopy of the purified bimolecular complex (CVF,Bb) and its isolated subunits, CVF and Bb. Negatively stained CVF imaged as an irregularly shaped cylindrical structure, with approximate dimensions of 137
C A, Smith   +2 more
openaire   +2 more sources

Complement system part I - molecular mechanisms of activation and regulation

open access: yesFrontiers in Immunology, 2015
Complement is a complex innate immune surveillance system, playing a key role in defense against pathogens and in host homeostasis. The complement system is initiated by conformational changes in recognition molecular complexes upon sensing danger ...
Nicolas eMerle   +3 more
doaj   +1 more source

Structural insights into C3 convertase activity of the classical pathway of complement. [PDF]

open access: yesNat Commun
Immune protection by the complement system depends on C3 cleavage by C3 convertases that is critical to all three activation pathways. Structural data on convertase formation in the classical pathway and on C3-substrate binding to convertases is lacking.
De la O Becerra KI   +3 more
europepmc   +2 more sources

Staphylococcus aureus proteins Sbi and Efb recruit human plasmin to degrade complement C3 and C3b

open access: yes, 2012
Upon host infection, the human pathogenic microbe Staphylococcus aureus (S. aureus) immediately faces innate immune reactions such as the activated complement system. Here, a novel innate immune evasion strategy of S. aureus is described.
Peter F. Zipfel   +17 more
core   +1 more source

The Role of Properdin in C5 Convertase Activity and C5b-9 Formation in the Complement Alternative Pathway

open access: yes, 2021
Contains fulltext : 242823.pdf (Publisher’s version ) (Open Access)The complement system is an important part of innate immunity. Complement activation leads to formation of convertase enzymes, switch of their specificity from C3 to C5 ...
Heuvel, L.P.W.J. van den   +5 more
core   +1 more source

Decay accelerating factor (CD55) protects neuronal cells from chemical hypoxia-induced injury

open access: yesJournal of Neuroinflammation, 2010
Background Activated complement system is known to mediate neuroinflammation and neurodegeneration following exposure to hypoxic-ischemic insults. Therefore, inhibition of the complement activation cascade may represent a potential therapeutic strategy ...
Tsokos George C   +5 more
doaj   +1 more source

image_1_Functional Characterization of Alternative and Classical Pathway C3/C5 Convertase Activity and Inhibition Using Purified Models.tif

open access: yes, 2018
Complement is essential for the protection against infections; however, dysregulation of complement activation can cause onset and progression of numerous inflammatory diseases.
Sanne Mol (5543531)   +8 more
core   +1 more source

Ischemia–Reperfusion Injury: Molecular Mechanisms and Therapeutic Interventions

open access: yesMedComm, Volume 7, Issue 7, July 2026.
Multiorgan ischemia–reperfusion injury begins with ischemia‐induced ATP depletion and ionic imbalance, followed by reperfusion‐triggered mitochondrial ROS/RNS bursts, regulated cell death, and DAMP release. Sterile inflammation converges on endothelial–immune–coagulation crosstalk, where NETs drive immunothrombosis, no‐reflow, and remote organ injury ...
Peng An   +4 more
wiley   +1 more source

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