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1 nt mice had elevated serum concentrations of glucose-6-phosphate isomerase.
2 induction of autoantibodies directed against glucose-6-phosphate isomerase.
4 se and reduced deposition of pathogenic anti-glucose-6-phosphate isomerase Abs in the joint (with a r
6 These genes encode enzymes in glycolysis (glucose-6-phosphate isomerase and phosphoglycerate mutas
7 inefficient at taking up the key autoantigen glucose-6-phosphate isomerase and that Msr1-deficient mi
8 to [6,6'-(3)H]Fru-2,6-P(2) using hexokinase, glucose-6-phosphate isomerase, and 6-phosphofructo-2-kin
9 elping B cells to produce arthritogenic anti-glucose-6-phosphate isomerase (anti-GPI) autoantibodies.
10 6.TCR.Calpha(-/-)H-2(b/g7) mice induced anti-glucose 6-phosphate isomerase antibody-dependent chronic
11 uld not be reproduced by increasing the anti-glucose-6-phosphate isomerase antibody load, which demon
12 mber of the IL-1 family, can exacerbate anti-glucose-6-phosphate isomerase autoantibody-induced arthr
13 e model of arthritis, autoantibodies against glucose-6-phosphate isomerase cause joint-specific infla
14 osure, twice-a-day treatment with 17l in the glucose-6-phosphate isomerase chronic in vivo mouse mode
18 atoid arthritis, autoantibodies specific for glucose-6-phosphate isomerase (GPI) can transfer joint-s
19 the transfer of autoantibodies specific for glucose-6-phosphate isomerase (GPI) into naive mice rapi
21 ceptors (BCRs) with different affinities for glucose-6-phosphate isomerase (GPI) were examined in the
22 vealed a point mutation, Gly-189 --> Glu, in glucose-6-phosphate isomerase (GPI), a glycolytic enzyme
23 om pathogenic immunoglobulins that recognize glucose-6-phosphate isomerase (GPI), a glycolytic enzyme
24 high titers of antibodies against the enzyme glucose-6-phosphate isomerase (GPI), promoted by CD4(+)
25 autoimmune arthritis by tracking the fate of glucose-6-phosphate isomerase (GPI)-reactive CD4(+) T ce
30 B cells both recognize the glycolytic enzyme glucose-6-phosphate-isomerase (GPI) as an autoantigen.
31 nize the ubiquitously expressed self-antigen glucose-6-phosphate-isomerase (GPI) initiates an anti-GP
34 y passive transfer of autoantibodies against glucose 6-phosphate isomerase is transient and therefore
35 ormation and autoantibody production against glucose-6-phosphate isomerase, leading to joint inflamma
36 thal phenotype of RNAi-mediated depletion of glucose-6-phosphate isomerase (PGI) in the glucose-deple
38 .5 +/- 0.5 %ID/g), as early as 1 d after the glucose-6-phosphate-isomerase serum injection, a time po
39 icro-positron emission tomography that these glucose-6-phosphate isomerase-specific autoantibodies ra
42 e in the titer of serum antibodies targeting glucose-6-phosphate isomerase, the relevant autoantigen,
43 (2) died in galactose medium as well as when glucose-6-phosphate isomerase was knocked down, suggesti
44 ransgenic mice specific for the self-antigen glucose-6-phosphate isomerase, we show that autoreactive
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