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1 tions for large mutation rates and including back mutations.
2 ecise for small mutation rates and excluding back mutations.
3 n colonies of a given size in the absence of back-mutations.
4                                         Both back mutation and compensatory mutations contributed to
5   Conversely, the NRY is less susceptible to back mutations and saturation, and is potentially more i
6  in models of interference among forward and back mutations at large numbers of sites on a nonrecombi
7 nce in recombinant Candid#1 viruses requires back-mutation at two positions specific to the Candid#1
8 oquine susceptibility is not the result of a back mutation in a formerly resistant parasite or a new
9                                      A V144M back mutation in SCaM-1 significantly restored its abili
10 over, there has been some recent evidence of back mutations in cancer: this phenomenon is currently w
11 -term dynamics of mutants in the presence of back-mutations is also addressed.
12                     By sequence analysis and back mutation, it was determined that the observed antag
13 which all characters are binary and in which back-mutations occur only at hybrid vertices.
14 nd binding affinity to parental MMGZ01 after back mutation of 12 canonical murine residues in the FRs
15 case with primary platinum resistance showed back mutation of BRCA1 in the primary tumor and showed a
16  approach in combination with the occasional back mutation of rare amino acids to consensus results i
17              Fitness recovery did not entail back mutations or compensatory mutations, but instead, w
18              Revertant mosaicism due to true back mutations or second-site mutations has been identif
19  genotypic reversion, most likely because of back mutation, originated in a lymphohematopoietic stem
20       In particular, with equal forward- and back-mutation rates, if division-controlled and a death-
21 merged due to continued evolution of pol and back mutation rather than through emergence of an archiv
22                                              Back mutations resulting in restoration of wild-type seq
23 ermining the DFE, such as protein stability, back-mutations, species complexity, and mutational robus
24              In some circumstances (ignoring back mutations) stable internal steady-state values for
25                                              Back mutation to germline sequence provided evidence for
26                                           If back-mutation to F427 offers an accessible pathway to in
27 hich a compensatory mutation, instead of the back mutation, was acquired to recover fitness.