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1 specific DNA molecules covering the complete microsatellite sequence.
2 controls and nontransfected cells in either microsatellite sequence.
3 ector sensitive to frameshift mutations in a microsatellite sequence.
4 ntegral numbers of dinucleotide repeats in a microsatellite sequence.
5 very two consecutive GGAA-repeats on shorter microsatellite sequences.
6 , RFX knockdown cells display instability in microsatellite sequences.
7 d markers by characterization of Xiphophorus microsatellite sequences.
8 NA polymerase errors in vitro using template microsatellite sequences.
9 haracterized by repeat length alterations at microsatellite sequences.
10 omyces cerevisiae contains numerous unstable microsatellite sequences.
11 cleotide mismatches and slippage mistakes at microsatellite sequences.
12 of many vertebrate genomes are comprized of microsatellite sequences.
13 e a major factor in promoting instability of microsatellite sequences.
14 ave been found to exhibit instability of DNA microsatellite sequences.
15 tor phenotype in these tumors extends beyond microsatellite sequences.
16 ucleotide, dinucleotide, and tetranucleotide microsatellite sequences.
17 es, including the well-studied P. falciparum microsatellite sequences, are commonly classified as VNT
18 air deficiency causes genetic instability at microsatellite sequences because of the cell's inability
19 nes were shown to be modified genetically in microsatellite sequences by MNU and are believed to have
21 mechanism different from the instability in microsatellite sequences caused by defects in mismatch r
22 pression required preservation of the TGFBR2 microsatellite sequence; cells in which this sequence wa
27 dually increased to include up to 67% of the microsatellite sequences examined after 19 to 20 weeks o
29 ome oxidase I gene, nine polymorphic nuclear microsatellites, sequences from 11 single-copy nuclear m
32 lustrate (i) the reduction of instability at microsatellite sequences, (ii) a significant decrease in
33 en used to determine mutation rates within a microsatellite sequence in human cancer cell lines with
35 nstability (MSI-H) accumulate mutations at a microsatellite sequence in the gene encoding transformin
40 ed by widespread insertions and deletions in microsatellite sequences, including those comprised of m
41 [GT/CA](10), [TC/AG](11) and [TTCC/AAGG](9) microsatellite sequences inserted in the herpes simplex
43 t strains, the vector containing the (A)(10) microsatellite sequence of TGFBR2 had a mutation rate (m
44 lbeta) error frequencies were quantitated in microsatellite sequences, relative to frame-shift error
45 the in vitro polymerase error frequencies at microsatellite sequences representative of those found i
46 f TGFBR2 with a 1-nucleotide deletion at its microsatellite sequence still produced a full-length TGF
47 ultiple human tumor suppressor genes include microsatellite sequences that are prone to mutations.
50 The mutational expansion of triplet repeat microsatellite sequences underlies the transmission of a
51 polymerase-DNA interactions as a function of microsatellite sequence, using polypyrimidine/polypurine
52 had deletions of a single CA-repeat from the microsatellite sequence, whereas repair-proficient cells
53 tions that were localized exclusively to the microsatellite sequences, whereas DNA damage by UV or N-
54 ave utilized this site to insert a synthetic microsatellite sequence within the beta-lactamase gene a
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