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1 d recombination in the germline and revealed somatic recombination.
2 that the mechanism of LOH at APC is probably somatic recombination.
3 e of Apc in tumors can proceed by homologous somatic recombination.
4 ls, where mu2 mutations cause an increase in somatic recombination.
5 through loss of heterozygosity by homologous somatic recombination.
6 ression in these lines is indeed a result of somatic recombination.
7 at this mutation can arise through errors in somatic recombination, an extremely unusual mutation mec
8 t extent the diverse Ig arsenal generated by somatic recombination and diversification is actually us
11 coded in the genome rather than generated by somatic recombination and that recognize either classica
12 T cell development including proliferation, somatic recombination, and thymic selection can be mappe
13 erse antigen receptors that are generated by somatic recombination, arose approximately 500 Mya at th
14 ccur by loss of heterozygosity (LOH) through somatic recombination between homologs presents an oppor
16 irst evidence that uniparental disomy due to somatic recombination constitutes one of the mechanisms
17 earrangements reported here, NF1REP-mediated somatic recombination could be an important mechanism fo
18 tion SNP genotyping technique has revealed a somatic recombination event-uniparental disomy, leading
19 to be nonrandom, have the characteristics of somatic recombination events and may define an important
21 ere able to observe an interesting effect on somatic recombination events in thalassemic embryos.
23 ion of LOH on chromosome 4 that occurred via somatic recombination/gene conversion, generating a regi
25 the kidneys express the immunoglobulin gene somatic recombination machinery usually restricted to hi
26 explain how a recently discovered example of somatic recombination occurred in an A188/W64A hybrid.
27 knockdown of candidate genes either through somatic recombination of floxed alleles or by direct del
29 al repertoire of AgRs is established through somatic recombination of V, D, and J gene segments durin
31 e-dependent epigenetic changes, conservative somatic recombination, or direct effects of alleles in t
33 diversity (D), and joining (J), that undergo somatic recombination to create diverse binding specific
34 tiated by loss of heterozygosity by means of somatic recombination, tumors form preferentially in the
35 in tandem with the normal exon (and prone to somatic recombination, which inactivates the gene) suppo
36 mbination is a tightly controlled process of somatic recombination whose regulation is mediated in pa
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