نتایج جستجو برای: complement activation

تعداد نتایج: 489504  

Journal: :Thrombosis and haemostasis 2012
Hongjie Wang Ilya Vinnikov Khurrum Shahzad Fabian Bock Satish Ranjan Juliane Wolter Muhammed Kashif Jun Oh Angelika Bierhaus Peter Nawroth Michael Kirschfink Edward M Conway Thati Madhusudhan Berend Isermann

Coagulation and complement regulators belong to two interactive systems constituting emerging mechanisms of diabetic nephropathy. Thrombomodulin (TM) regulates both coagulation and complement activation, in part through discrete domains. TM's lectin like domain dampens complement activation, while its EGF-like domains independently enhance activation of the anti-coagulant and cytoprotective ser...

Journal: :Immunobiology 2010
Russell Wallis Daniel A Mitchell Ralf Schmid Wilhelm J Schwaeble Anthony H Keeble

Understanding the structural organisation and mode of action of the initiating complex of the classical pathway of complement activation (C1) has been a central goal in complement biology since its isolation almost 50 years ago. Nevertheless, knowledge is still incomplete, especially with regard to the interactions between its subcomponents C1q, C1r and C1s that trigger activation upon binding ...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2003
Riina Oksjoki Hanna Jarva Petri T Kovanen Petri Laine Seppo Meri Markku O Pentikäinen

OBJECTIVE Complement activation has been suggested to play a role in atherogenesis. To study the regulation of complement activation in human coronary atherosclerotic lesions, we examined the spatial relationships between the major complement inhibitor, factor H, and the complement activation products C3d and C5b-9. METHODS AND RESULTS In early lesions (American Heart Association types II and...

Journal: :The Journal of clinical investigation 2006
Joshua M Thurman Danica Ljubanović Pamela A Royer Damian M Kraus Hector Molina Nicholas P Barry Gregory Proctor Moshe Levi V Michael Holers

Ischemia/reperfusion (I/R) of several organs results in complement activation, but the kidney is unique in that activation after I/R occurs only via the alternative pathway. We hypothesized that selective activation of this pathway after renal I/R could occur either because of a loss of complement inhibition or from increased local synthesis of complement factors. We examined the relationship b...

Journal: :Circulation 1999
C S Rinder H M Rinder K Johnson M Smith D L Lee J Tracey G Polack P Higgins C G Yeh B R Smith

BACKGROUND We previously demonstrated that inhibiting formation of terminal complement components (C5a and C5b-9) prevents platelet and neutrophil (PMN) but not monocyte activation during simulated extracorporeal circulation (SECC). This study examined whether earlier complement inhibition during SECC, blocking C3a formation, would additionally prevent monocyte activation. METHODS AND RESULTS...

2010
E. J. Shannon F. G. Sandoval M. J. Morales

One inflammatory event that may be involved in erythema nodosum leprosum (ENL) is the activation of complement, and thalidomide could suppress ENL by inhibiting its activation. To determine if thalidomide inhibits the activation of complement, we first incubated normal serum with Mycobacterium leprae or with zymosan in the presence of thalidomide. Residual functional complement was then determi...

Journal: :Protein science : a publication of the Protein Society 2008
Nurit Haspel Daniel Ricklin Brian V Geisbrecht Lydia E Kavraki John D Lambris

The C3-inhibitory domain of Staphylococcus aureus extracellular fibrinogen-binding protein (Efb-C) defines a novel three-helix bundle motif that regulates complement activation. Previous crystallographic studies of Efb-C bound to its cognate subdomain of human C3 (C3d) identified Arg-131 and Asn-138 of Efb-C as key residues for its activity. In order to characterize more completely the physical...

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