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1 nd has ligand specificity similar to that of mannan-binding lectin.
2 ly reported for the lectin homologs SP-D and mannan-binding lectin.
3 way and absence of the LP complement protein mannan-binding lectin abrogates elastase-induced AAA.
6 n pathway deficiency, a mouse strain lacking mannan-binding lectin-associated serine protease-2 (MASP
7 mediated by direct cleavage of native C3 by mannan-binding lectin-associated serine protease-2 bound
11 lecules leading to the activation of zymogen mannan-binding lectin-associated serine proteases (MASPs
12 H-ficolin is found in plasma associated with mannan-binding lectin-associated serine proteases (MASPs
13 ternative pathway and mannan-binding lectin, mannan-binding lectin-associated serine proteases 1 and
14 In serum, CL-L1 was found in complexes with mannan-binding lectin-associated serine proteases, sugge
15 anism, which is conserved in C1r and also in mannan-binding lectin-associated serine proteases, the s
16 eir binding by recognition molecules such as mannan-binding lectin, C-reactive protein and the mannos
17 in pathway (LP) showed that both ficolin and mannan-binding lectin can activate the LP through natura
18 ution of blistering had a similar pattern in mannan-binding lectin-deficient and control mice and was
19 ys in this model, we injected C1q-deficient, mannan-binding lectin-deficient, and factor B-deficient
20 he lectin activation pathway upon binding of mannan-binding lectin, ficolins, or collectin kidney 1 (
22 and factor H in the alternative pathway and mannan-binding lectin, mannan-binding lectin-associated
26 nt, the pattern recognition molecules (PRMs) mannan-binding lectin (MBL) and ficolins complexed with
28 In teleost fish, the immune functions of mannan-binding lectin (MBL) associated protein (MAP) and
33 b, CR1 was reported to interact with C1q and mannan-binding lectin (MBL) likely through its C-termina
35 ght to occur via recognition of pathogens by mannan-binding lectin (MBL) or ficolins in complex with
36 activation by Neisseria gonorrhoeae via the mannan-binding lectin (MBL) pathway in normal human seru
39 t the soluble pattern recognition molecules, mannan-binding lectin (MBL), L-ficolin, and M-ficolin, w
41 ction of an endogenous complement inhibitor, mannan-binding lectin (MBL)-associated protein (MAp)44,
45 found that the C7 rs6876739 CC genotypes and mannan-binding lectin (MBL2) gene polymorphisms of liver
49 lement components revealed that C1q, but not mannan-binding lectin, was required for complement activ
50 etic deficiency in early complement, IgM, or mannan-binding lectin were characterized in a mesenteric
51 to ischemic Ag providing a binding site for mannan-binding lectin which subsequently leads to activa
52 to the same areas that stain positively for mannan-binding lectin, which suggests that the complemen
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