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  • ELISA
  • A ) Complement FH levels in mouse plasma isolated from 19 C3KI mice (triangles), 34 C3KI/WT (squares), and 19 WT (circle) mice, P14-28, were established using an in-house sandwich ELISA described in Methods. (jci.org)
  • B ) C5 levels in mouse plasma isolated from 17 C3KI, 15 C3KI/WT, and 8 WT mice on P14-P28 were established using an in-house sandwich ELISA. (jci.org)
  • gene
  • Recently, we identified the gene that encoded complement factor C5 as a quantitative trait gene that modifies the course of hepatic fibrosis ( 16 ). (asnjournals.org)
  • To determine the frequency of specific disease-associated C5 and C6 gene mutations in patients presenting with MD in the Western Cape. (scielo.org.za)
  • complexes
  • Through development of a highly purified model system for C5 convertases, we here aim to provide insights into the surface-specific nature of these important protease complexes. (biomedcentral.com)
  • C4b2a is the widely used short‐hand nomenclature for the C4b-C2a complex in the complement field, and similar nomenclature is used for the remaining complexes in the following). (embopress.org)
  • Molecular
  • So far, it has been difficult to study the exact molecular arrangement of C5 convertases, because their non-catalytic subunits (C3b) are covalently linked to biological surfaces through a reactive thioester. (biomedcentral.com)
  • The developed model and molecular insights are essential to understand the molecular basis of deregulated complement activity in human disease and will facilitate future design of therapeutic interventions against these critical enzymes in inflammation. (biomedcentral.com)
  • Human
  • It is also known to be very species-specific for human C5, despite an important degree of conservation of the targeted macroglobulin domain, MG7, with that of other primates. (innopsys.com)
  • vivo
  • Thus, our data provide in vivo modeling evidence that gain-of-function changes in complement C3 drive aHUS. (jci.org)
  • mice
  • This study investigated the role of C5 in the development of renal tubulointerstitial fibrosis by ( 1 ) induction of renal fibrosis in wild-type and C5 −/− mice by unilateral ureteral ligation (UUO) and ( 2 ) investigation of the effects of a C5a receptor antagonist (C5aRA) in UUO. (asnjournals.org)
  • In C5 −/− mice, when compared with wild-type controls, markers of renal fibrosis (Sirius Red, type I collagen, fibronectin, α-smooth muscle actin, vimentin, and infiltrating macrophages) were significantly reduced on day 5 of UUO. (asnjournals.org)
  • Cortical mRNA of all PDGF isoforms and of TGF-β 1 ( i.e. , central mediators of renal disease) were significantly reduced in C5 −/− mice when compared with controls. (asnjournals.org)
  • We used DBA2/J mice, which are genetically deficient in complement C5. (spandidos-publications.com)
  • DBA1/J mice have a normal complement system, and were used as controls. (spandidos-publications.com)
  • The development of DSS colitis was aggravated in genetically C5-deficient DBA2/J mice. (spandidos-publications.com)
  • Thus
  • Thus, aHUS provides an archetypal complement-mediated disease with which to model new therapeutic strategies and treatments. (jci.org)
  • In order to permeabilize both the bacterial outer and inner membrane and thus kill a bacterium, MACs need to be assembled locally by the C5 convertase enzymes. (bioportfolio.com)
  • therapeutic
  • Using a combined genetic and pharmacologic approach, C5, in particular C5a, is identified as a novel profibrotic factor in renal disease and as a potential new therapeutic target. (asnjournals.org)