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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 hy donors versus BTK-deficient patients with X-linked agammaglobulinemia.
7 witzerland was 1.3:100,000, almost double of X-linked agammaglobulinemia.
8 B-cell levels; prior anti-CD20 therapy, and X-linked agammaglobulinemia.
9 tions in the human btk gene are the cause of X-linked agammaglobulinemia, a male immune deficiency di
10 owest response was detected in patients with X-linked agammaglobulinemia and in patients with CVID wi
12 Bruton's tyrosine kinase (Btk) causes human X-linked agammaglobulinemia and murine X-linked immunode
13 ain pathological conditions such as myeloma, X-linked agammaglobulinemia, and HIV infection may provi
14 mmune Deficiency, leukocyte adhesion defect, X-linked agammaglobulinemia, Ataxia Telangiectasia, Hype
15 such as common variable immunodeficiency and X-linked agammaglobulinemia, bacterial organisms are the
16 isolated or undefined antibody deficiencies, X-linked agammaglobulinemia, combined B- and T-cell immu
17 e present the case of a 34-year-old man with X-linked agammaglobulinemia from Australia suffering fro
18 (Btk), which is mutated in the human disease X-linked agammaglobulinemia, has been shown to interact
19 utation in the PH-TH domain (R28H) linked to X-linked agammaglobulinemia impairs BTK activation at th
20 hat results in the immunodeficiency diseases X-linked agammaglobulinemia in humans and X-linked immun
21 illustrated by the primary immune disorder, X-linked agammaglobulinemia in which patients are prone
22 sine kinase (Btk) result in a disease called X-linked agammaglobulinemia, in which there is a profoun
24 other BCR signaling deficiencies, including X-linked agammaglobulinemia, our findings suggest that C
25 Bruton's tyrosine kinase (Btk) is mutated in X-linked agammaglobulinemia patients and plays an essent
28 dicated by the X-linked immunodeficiency and X-linked agammaglobulinemia phenotypes of mice and men t
31 e development of gene therapy strategies for X-linked agammaglobulinemia, the immunodeficiency associ
32 tor activation was reported in patients with X-linked agammaglobulinemia, underscoring the important
33 sine kinase (BTK) mutations as the cause for X-linked agammaglobulinemia was a milestone in understan
34 dition, a patient previously thought to have X-linked agammaglobulinemia was found to have an amino a
35 mutation of the Btk PH domain, which causes X-linked agammaglobulinemia, was introduced into the flu
37 obulinemia and absent B cells are males with X-linked agammaglobulinemia, which is caused by mutation
38 Control of N addition appears aberrant in X-linked agammaglobulinemia, which may exacerbate the bl
39 -cell development and patients with presumed X-linked agammaglobulinemia who did not have mutations i
40 Severe combined immunodeficiency (SCID) and X-linked agammaglobulinemia (XLA) are inborn errors of i
42 h an inherited lack of mature B cells, i.e., X-linked agammaglobulinemia (XLA) displayed highly funct
44 ficient mice or monocytes from patients with X-linked agammaglobulinemia (XLA) exhibited increased NL
47 because mutations in Btk are responsible for X-linked agammaglobulinemia (XLA) in humans and X-linked
48 ion of Bruton's tyrosine kinase (Btk) causes X-linked agammaglobulinemia (XLA) in humans and X-linked
49 in Bruton's tyrosine kinase (Btk) result in X-linked agammaglobulinemia (XLA) in humans and X-linked
50 e (btk) cause the B cell deficiency diseases X-linked agammaglobulinemia (XLA) in humans and X-linked
51 Btk result in the B cell immunodeficiencies X-linked agammaglobulinemia (XLA) in humans and X-linked
52 Btk result in the B cell immunodeficiencies X-linked agammaglobulinemia (XLA) in humans and X-linked
53 he Bruton's tyrosine kinase (btk) gene cause X-linked agammaglobulinemia (XLA) in humans and X-linked
62 phoblastoid lines derived from patients with X-linked agammaglobulinemia (XLA) lacking Btk expression
63 lines, and cultured cells from patients with X-linked agammaglobulinemia (XLA) suggested defective TL
65 eatment with wortmannin and in patients with X-linked agammaglobulinemia (XLA), a condition caused by
67 light key issues in gene therapy strategies: X-linked agammaglobulinemia (XLA), X-linked chronic gran
75 severe combined immune deficiency (SCID) and X-linked agammaglobulinemia (XLA); however, gain-of-func