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1 tigen receptor loci and the discovery of the recombination activating gene-1.
2 regulatory conditions caused by mutations in recombination activating gene 1/2 (RAG 1/2), IL-2 recept
3 th patients with T(-)B(-)NK(+)SCID caused by recombination activating gene 1/2 (RAG1/2) deficiencies.
4 During the maturation of pre-B cells, the recombination activating gene 1 and 2 (RAG1/2) endonucle
6 e recombination signal sequences targeted by recombination activating genes 1 and 2 during antigen re
7 cleavage step of V(D)J recombination by the recombination-activating gene 1 and 2 (RAG1/2) proteins
8 ntigen receptors by the reactivation of RAG (recombination-activating gene)1 and RAG2 and secondary V
9 RSSs) requires the coordinated action of the recombination-activating genes 1 and 2 (RAG1/RAG2) recom
11 cess mediated by several proteins, including recombination-activating genes 1 and 2, RAG1 and RAG2.
13 ymphoblastic leukemia (T-ALL) model onto the recombination-activating gene 1(-/-) background, we show
16 y the transplantation of a segment of RAG-1 (recombination-activating gene 1) deficient intestine, wh
17 and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag-1(-/-)) m
18 es that are required for NEC development, as recombination activating gene 1-deficient (Rag1-/-) mice
19 ytes from severe combined immunodeficient or recombination activating gene 1-deficient mice expressed
20 Although the acquired phenotype is stable in recombination activating gene-1-deficient (RAG-/-) recip
21 fusion in wild-type mice (P<0.01) but not in recombination activating gene-1-deficient mice (P<0.05).
24 IL-10) produced by CD11b(+) myeloid cells in recombination-activating gene 1-deficient (Rag1(-/-)) re
25 ive transfer of IL-9(+)IL-10(+) T cells into recombination-activating gene 1-deficient mice induced c
26 umonitis was induced in C57BL/6 wild-type or recombination-activating gene 1-deficient mice treated p
28 efined amounts of naive TCR-transgenic (TCR) recombination-activating gene-1-deficient T cells into a
29 talytically inactive RAG1 (dominant-negative recombination activating gene 1 [dnRAG1] mice) that deve
30 es and T cells in both wild-type C57BL/6 and recombination activating gene 1-/- irradiated hosts.
32 macrophages derived from primitive yolk sac, recombination activating gene 1(+) lymphomyeloid, and Fm
38 oth cortical TEC subsets are also present in recombination activating gene 1 (RAG-1(-/-)) and TCRbeta
40 examined IEL from knockout mice lacking the recombination activating gene-1 (rag-1), CD3epsilon, or
41 nflammation, and T-cell adoptive transfer to recombination-activating gene 1 (Rag-1)(-/-) mice were u
42 ymic-deprived nude and old mice express less recombination-activating gene-1 (RAG-1) mRNA than they d
46 describe a third phenotype for mutations in recombination activating gene 1 (RAG1), in addition to t
47 ptor alpha (IL4Ra)-knockout mice, but not in recombination activating gene 1 (Rag1)-knockout mice dem
48 he assembly of antigen receptor genes by the recombination activating gene 1 (RAG1)-RAG2 (collectivel
51 nts and transcription control binding of the recombination-activating gene 1 (RAG1) and RAG2 proteins
54 vel insights into the origin and function of recombination-activating gene 1 (RAG1) and RAG2, the lym
58 PSCs) generated from patients with different recombination-activating gene 1 (RAG1) mutations to asse
61 in the DNA recombination machinery, such as recombination-activating gene 1 (RAG1), RAG2, or DNA cro
62 to the B cell lineage in the context of the recombination-activating gene 1 (RAG1)-deficient backgro
65 nduced demyelination were investigated using recombination-activating gene 1-/- (RAG1-/-) mice infect
66 studied Rag1 knockout mice deficient in the recombination activating gene 1 required for development
68 cells as a consequence of deletion of Rag1 (recombination-activating gene 1), with infection in norm