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1 ongenital asplenia, and 2 of Bruton disease (X-linked agammaglobulinemia).
2 cally normal in BTK, the gene that underlies X-linked agammaglobulinemia.
3 ptor signaling culminate in X-linked and non-X-linked agammaglobulinemia.
4 l blocks in human B-cell ontogeny leading to X-linked agammaglobulinemia.
5 ction and results in a clinical phenotype of X-linked agammaglobulinemia.
6 tions in the human btk gene are the cause of X-linked agammaglobulinemia, a male immune deficiency di
8 Bruton's tyrosine kinase (Btk) causes human X-linked agammaglobulinemia and murine X-linked immunode
9 ain pathological conditions such as myeloma, X-linked agammaglobulinemia, and HIV infection may provi
10 such as common variable immunodeficiency and X-linked agammaglobulinemia, bacterial organisms are the
11 e present the case of a 34-year-old man with X-linked agammaglobulinemia from Australia suffering fro
12 (Btk), which is mutated in the human disease X-linked agammaglobulinemia, has been shown to interact
13 hat results in the immunodeficiency diseases X-linked agammaglobulinemia in humans and X-linked immun
14 illustrated by the primary immune disorder, X-linked agammaglobulinemia in which patients are prone
15 sine kinase (Btk) result in a disease called X-linked agammaglobulinemia, in which there is a profoun
17 Bruton's tyrosine kinase (Btk) is mutated in X-linked agammaglobulinemia patients and plays an essent
19 dicated by the X-linked immunodeficiency and X-linked agammaglobulinemia phenotypes of mice and men t
22 e development of gene therapy strategies for X-linked agammaglobulinemia, the immunodeficiency associ
23 tor activation was reported in patients with X-linked agammaglobulinemia, underscoring the important
24 sine kinase (BTK) mutations as the cause for X-linked agammaglobulinemia was a milestone in understan
25 dition, a patient previously thought to have X-linked agammaglobulinemia was found to have an amino a
26 mutation of the Btk PH domain, which causes X-linked agammaglobulinemia, was introduced into the flu
28 obulinemia and absent B cells are males with X-linked agammaglobulinemia, which is caused by mutation
29 Control of N addition appears aberrant in X-linked agammaglobulinemia, which may exacerbate the bl
30 -cell development and patients with presumed X-linked agammaglobulinemia who did not have mutations i
31 Severe combined immunodeficiency (SCID) and X-linked agammaglobulinemia (XLA) are inborn errors of i
35 because mutations in Btk are responsible for X-linked agammaglobulinemia (XLA) in humans and X-linked
36 ion of Bruton's tyrosine kinase (Btk) causes X-linked agammaglobulinemia (XLA) in humans and X-linked
37 in Bruton's tyrosine kinase (Btk) result in X-linked agammaglobulinemia (XLA) in humans and X-linked
38 e (btk) cause the B cell deficiency diseases X-linked agammaglobulinemia (XLA) in humans and X-linked
39 Btk result in the B cell immunodeficiencies X-linked agammaglobulinemia (XLA) in humans and X-linked
40 Btk result in the B cell immunodeficiencies X-linked agammaglobulinemia (XLA) in humans and X-linked
41 he Bruton's tyrosine kinase (btk) gene cause X-linked agammaglobulinemia (XLA) in humans and X-linked
48 phoblastoid lines derived from patients with X-linked agammaglobulinemia (XLA) lacking Btk expression
49 lines, and cultured cells from patients with X-linked agammaglobulinemia (XLA) suggested defective TL
51 eatment with wortmannin and in patients with X-linked agammaglobulinemia (XLA), a condition caused by
59 severe combined immune deficiency (SCID) and X-linked agammaglobulinemia (XLA); however, gain-of-func
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