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1 e-strand break is introduced next to a short inverted repeat sequence.
2 including a long spacer region containing an inverted repeat sequence.
3 involving homologous recombination of short inverted repeat sequences.
4 ten occur at short direct repeats that flank inverted repeat sequences.
5 bp in size and is bordered by 20-bp terminal inverted repeat sequences.
6 ity of target sites had no mismatches in the inverted repeat sequences.
7 t levels of homologous recombination between inverted repeat sequences.
8 ons that self-assemble from single identical inverted-repeat sequences.
9 abilizing this recombination intermediate in inverted-repeat sequences.
11 ylated PmrA bind to a 16-base pair imperfect inverted repeat sequence (5'-TTAAKTTCTTAAKGTT-3'), which
12 tified DNA-protein contact points at a novel inverted repeat sequence (AACCACTGGTT) and an Ets-like r
13 of replication between the arms of a GC-rich inverted repeat sequence adjacent to the binding site fo
14 n integrate both short oligonucleotides with inverted repeat sequences and a 2.8 kb excised mini-casp
16 -helix DNA-binding motif, recognizes a 19-bp inverted repeat sequence, and has a typical DNase I foot
17 owed in Saccharomyces cerevisiae that nearby inverted repeat sequences ( approximately 20-200 bp of h
18 taining many copies of the viral genome with inverted repeat sequences at the junctions between monom
19 coelicolor A3(2) were found to have 1.06 Mb inverted repeat sequences at their termini (i.e. long-te
20 " class of mutations that arise in imperfect inverted repeat sequences by DNA-strand misalignments du
21 of interest: an RNA/DNA hybrid domain and an inverted repeat sequence capable of forming a stem-loop
23 ent here the single-crystal structure of the inverted repeat sequence d(CCGGTACCGG) as a Holliday jun
24 Ser beta-sheet that binds specifically to an inverted repeat sequence distinct from those recognized
26 a cruciform DNA structure formed by a 60 bp inverted repeat sequence embedded in a negatively superc
28 ally to oriV DNA at several sites containing inverted repeat sequences (i.e., IR-1) and nonspecifical
30 sin occurred via binding directly to a short inverted repeat sequence in the intergenic region overla
32 otein in various genetic backgrounds, and an inverted repeat sequence in the promoter of hetP was nec
33 R binds specifically and tightly to an 11-bp inverted repeat sequence in the promoter regions of the
34 lis OhrR binds cooperatively to two adjacent inverted repeat sequences in the ohrA control region and
35 pression of the operon by binding to several inverted repeat sequences in the promoter region, dnaKp.
36 spR confers repression by binding to several inverted repeat sequences in the promoter region, dnaKp.
38 rs and head-to-tail (h-t) concatemers within inverted repeat sequences (IRs) near probable origins of
39 One, O(C), which includes a 20-bp imperfect inverted-repeat sequence, is located between the two pro
43 he Tcr3 element contained imperfect terminal inverted repeat sequences of 56 bp and created a 2 bp ta
45 data suggest that ToxR is not recognizing an inverted repeat sequence per se in the activation of tox
47 nce is remarkably similar to a related 7-1-7 inverted repeat sequence recognized by PerR, a Fur paral
49 ly, deletion of a 26-bp region containing an inverted repeat sequence resulted in the loss of express
50 f the short transcript mapped adjacent to an inverted repeat sequence, suggesting that the sequence c
52 mRNA from the usd-spoIIID operon contains an inverted repeat sequence that is predicted to form a ste
53 for ohrA transcription identifies a perfect inverted repeat sequence that is required for OhrR-media
55 tprinting demonstrated binding of CouR to an inverted repeat sequence that overlaps the -10 region of
56 0-generated duplications are all symmetrical inverted repeat sequences that are apparently derived fr
57 d homologous recombination between the large inverted repeat sequences that exist in the genome, rath
61 ection" mechanism that can restore mutilated inverted-repeat sequences to a palindrome at the Ori of
62 posase binds specifically to ISY100 terminal inverted repeat sequences via an N-terminal DNA-binding
64 sses a single operon by binding to a perfect inverted repeat sequence, whereas HpNikR binds to promot
65 Upstream of each putative promoter is an inverted repeat sequence which resembles a similar eleme
66 he catA86 coding sequence contains a pair of inverted repeat sequences which cause sequestration of t
68 d oligonucleotide conjugates to hybridize to inverted repeat sequences within supercoiled double-stra
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