ライフサイエンスコーパス: complement binding

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1 table surrogate marker for the prediction of complement binding.

2 hanced survival in human serum and decreased complement binding.

3 intrinsically disordered, and is involved in complement binding.

4 by tumor necrosis factor alpha and inhibits complement binding.

5 lex formation, a PXXP motif in HPK1 strongly complements binding.

6 against SHIV challenge when Fc receptor and complement-binding activities are engineered out of the

7 rescence-to-cutoff ratios >5 correlated with complement binding activity, whereas values <5 denoted c

8 tivity is associated with the elimination of complement binding alone.

9 e protection of the nanocarrier surface from complement binding and activation.

10 Compared with the strong complement binding and CDC with Abs against glycolipids

11 35A, P329G (LALA-PG) variant that eliminates complement binding and fixation as well as Fc-gamma-depe

12 -, and IgG-Luminex, to assess or predict the complement-binding capability of HLA IgG antibodies.

13 High levels of anti-HLA antibodies and their complement binding capacity were associated with increas

14 We investigated whether the complement-binding capacity of anti-HLA antibodies plays

15 Assessment of the complement-binding capacity of donor-specific anti-HLA a

16 donor-specific anti-HLA antibodies and their complement-binding capacity.

17 m of this study was to determine the further complement-binding characteristics of the most harmful D

18 The extracellular complement-binding (CUB) and coagulation factor domains

19 main binds to the amino-terminal quarter, or complement-binding (CUB) domain, of Npn-1.

20 m protease inhibitor that contains potential complement-binding domains, and has been shown to improv

21 al (54%), as compared with patients with non-complement-binding donor-specific anti-HLA antibodies (9

22 The presence of complement-binding donor-specific anti-HLA antibodies af

23 Patients with complement-binding donor-specific anti-HLA antibodies af

24 Adding complement-binding donor-specific anti-HLA antibodies to

25 The presence of de novo persistent, complement-binding DQ DSA negatively impacts kidney allo

26 tation detection, monitoring, and removal of complement-binding DQ might be crucial for improving lon

27 Solid-phase assays to distinguish complement binding from noncomplement binding HLA-specif

28 ck of antiinflammatory IgA, and an excess of complement-binding IgG and IgM Abs, will promote inflamm

29 sult does not indicate the absence of strong complement-binding IgG subclasses.

30 an fluorescence intensity [MFI]>500), strong complement-binding IgG1 and IgG3 subclasses accounted fo

31 ves prediction of C1q binding likely because complement-binding IgG1 and IgG3 subclasses dominate reg

32 man leukocyte antigen antibodies with strong complement-binding IgG1 and IgG3 subclasses.

33 Neither complement binding in vitro nor antigen-antibody binding

34 nst microbes, such as opsonophagocytosis and complement binding, negatively correlated with antibody

35 One of these, extracellular complement binding protein (Ecb), is known to interfere

36 The virus encodes homologs to complement-binding proteins, three cytokines (two macrop

37 n was dose dependent and was reproduced in a complement binding reaction consisting of six purified p

38 ns, Fw contains a lectin-binding domain, ten complement binding repeats, and a transmembrane domain.

39 ket on the SH3C while several other residues complement binding through hydrophobic interactions, cre

40 treatment is likely due to the prevention of complement binding to aggregates or dissociation of aggr

41 rum samples from patients treated with IVIg, complement binding to and lysis of complement-sensitive

42 nd CDC with Abs against glycolipids and KSA, complement binding was diminished with Abs against mucin

43 During this period of time, IgM and complement binding were observed within the graft, as we

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