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1 ) structural variation that results in GPR42 copy number polymorphism.
2 Human defensin genes show marked copy-number polymorphism.
4 used on SNPs and, more recently, large-scale copy number polymorphisms and ectopic rearrangements.
6 recombination leading to genomic disorders, copy-number polymorphisms and gene and transcript innova
7 FA6, and DEFB1 are single copy, suggest that copy number polymorphisms are not a common feature of th
8 mplifications of the human genomic sequence (copy number polymorphisms) are the cause of numerous dis
9 mportant for identifying naturally occurring copy number polymorphisms as well as alterations that un
10 population genomic studies reporting rampant copy-number polymorphism at the intraspecific level.
11 es (T1D) found null associations with common copy number polymorphisms, but CNVs of low frequency and
12 ears ago, but the extent and implications of copy number polymorphism (CNP) have only recently become
14 continents, and we identified 119 regions of copy-number polymorphism (CNP), 73 of which were previou
18 ion) informed by integer genotypes for 1,320 copy number polymorphisms (CNPs) that segregate at an al
19 assigns copy number across regions of common copy number polymorphisms (CNPs), calls genotypes of SNP
21 discoveries have shown that several of these copy-number polymorphisms (CNPs) are associated with hum
22 arrays to create a fine-scale genomic map of copy-number polymorphisms (CNPs) in Drosophila melanogas
23 attempt to assess the heritability and LD of copy-number polymorphisms (CNPs) in duplication-rich reg
27 etion, these breakpoint regions are sites of copy number polymorphism in controls, indicating that th
29 ylactic antibiotics, providing evidence that copy number polymorphisms in an antimicrobial peptide as
36 ity of a large number of recently discovered copy number polymorphisms is much higher than initially
37 oci evolve under purifying selection against copy number polymorphisms; (iv) genes that encode inhere
38 regions and primarily reflect constitutional copy number polymorphisms, many subtle imbalances were d
40 ng gene and that recognition of sequence and copy number polymorphism of the FFAR3/GPR42 complex be c
43 ion (CGH) for copy number changes and single-copy number polymorphism (SNP) microarrays for allelic l
45 use strains show comparable, if not greater, copy number polymorphism when compared to human; however
46 tic abnormalities not corresponding to known copy number polymorphisms, with all but two cases (96%)
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