ライフサイエンスコーパス: mispaired base

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1 ctivity of MutH in the absence of MutS and a mispaired base.

2 ded DNA or a control duplex DNA containing a mispaired base.

3 nitiate repair of DNA by excising damaged or mispaired bases.

4 ial binding of Msh2p-Msh6p to DNA containing mispaired bases.

5 em that is at least as high as it has as for mispaired bases.

6 ingle base pair sequence contexts around the mispaired bases.

7 SH3, and MSH6-function in MMR by recognizing mispaired bases.

8 ct replication- and recombination-associated mispaired bases and influence the stability of simple re

9 sh6-G1142D complex, the mutant complex binds mispaired bases and is defective for ATP-induced sliding

10 DNA mismatch repair corrects mispaired bases and small insertions/deletions in DNA.

11 resulted in an Msh2-Msh6 complex that bound mispaired bases but could not form sliding clamps or bin

12 The incorporation efficiency for mispaired bases by the L561A variant ranged from 1.5 x 1

13 rnary complexes with Mlh1-Pms1, and occludes mispaired bases from other mismatch repair pathways.

14 esponsible for strand-specific correction of mispaired bases has been highly conserved during evoluti

15 e which recognizes and cleaves DNA 5' to the mispaired base in a strand-specific manner.

16 MutS protein recognizes mispaired bases in DNA and targets them for mismatch rep

17 plicated DNA and is transferred from PCNA to mispaired bases in DNA.

18 eterodimer plays a key role in the repair of mispaired bases in DNA.

19 er arising from the formation of unpaired or mispaired bases in heteroduplex DNAs.

20 Repair of most modified and mispaired bases in the genome is initiated by DNA glycos

21 icted to cause a defect in the correction of mispaired bases inserted during DNA replication.

22 at hairpin formation involving ligation of a mispaired base is much faster for R169D than for wild-ty

23 D mutant complexes, the mutant complex binds mispaired bases, is defective for ATP-induced sliding cl

24 lexes with Mlh1-Pms1 that either occlude the mispaired base or prevent Mlh1-Pms1 from acting in alter

25 d incorporation efficiency (k(pol)/K(D)) for mispaired bases relative to the wild-type enzyme.

26 ncreases replication fidelity by eliminating mispaired bases resulting from replication errors.

27 overall fidelity of replication and targets mispaired bases that arise through replication errors, d

28 In a total of 57 (2.5%) mispaired bases, there was a strong bias to G.T, G.A, G.

29 ponent of replication centers independent of mispaired bases; this localized pool accounted for 10%-1

30 plication is sometimes compromized, allowing mispaired bases to persist and be incorporated into the

31 The MSH2-MSH6 complex bound to a mispaired base was found to be converted by ATP binding

32 charomyces cerevisiae MSH2-MSH6 complex with mispaired bases was analyzed using gel mobility shift as

33 Mlh1-Pms1 foci increased when the number of mispaired bases was increased; in contrast, Msh2-Msh6 fo

34 orate purine-purine or pyrimidine-pyrimidine mispaired bases which may be preferentially proofread by

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