戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 owth of spt8Delta and spt3Delta strains on 6-azauracil.
2 increased H4 acetylation and resistance to 6-Azauracil.
3 persensitivity to the anti-elongation drug 6-azauracil.
4 ene renders S. pombe sensitive to the drug 6-azauracil.
5 phenotypes and an increased sensitivity to 6-azauracil.
6  than wild type to the cytotoxic effect of 6-azauracil.
7 h sensitivity to growth in the presence of 6-azauracil.
8 s sensitive to growth on medium containing 6-azauracil.
9  to the transcription elongation inhibitor 6-azauracil.
10  adenine compounds, whereas derivatives of 5-azauracil (2,4-dioxotriazine) are known to form weak com
11  under 'transcriptional stress' induced by 6-azauracil (6-AU) and inactivation of pol II, TFIIE or CT
12 aterno-Buchi (aPB) reaction of lipids with 6-azauracil (6-AU) was proposed for the first time for the
13 but snz1 and sno1 mutants are sensitive to 6-azauracil (6-AU), an inhibitor of purine and pyrimidine
14  nhp6ab cells being extremely sensitive to 6-azauracil (6-AU).
15 s overexpression of the NOT4 gene elicited 6-azauracil (6AU) and mycophenolic acid sensitivities, hal
16                                      Using 6-azauracil (6AU) as an indicator of transcription elongat
17 ne enzyme in vitro, confers sensitivity to 6-azauracil (6AU), a drug that depresses cellular nucleosi
18 sensitivity to a drug that inhibits IMPDH, 6-azauracil (6AU), by a mechanism that is poorly understoo
19 sensitive to the nucleotide-depleting drug 6-azauracil (6AU).
20 tent, in wild-type (WT) cells treated with 6-azauracil (6AU).
21              Ulp2 loss sensitizes cells to 6-azauracil, a hallmark of transcriptional elongation defe
22       set2 deletion mutant is sensitive to 6-azauracil, a property often associated with impaired tra
23 y killed upon exposure to the base analogs 6-azauracil and 8-azahypoxanthine for 48 hr.
24 ring biologically relevant motifs, such as 6-azauracil and coumarin, delivering products with excelle
25 s in the Paf1 complex cause sensitivity to 6-azauracil and diminished PUR5 induction, properties freq
26    BUR1 mutants are sensitive to the drugs 6-azauracil and mycophenolic acid and interact genetically
27                                  The drugs 6-azauracil and mycophenolic acid reduce both the elongati
28 itive to inhibitors of this enzyme such as 6-azauracil and mycophenolic acid, at least partly because
29 t a deletion of RTF1 causes sensitivity to 6-azauracil and mycophenolic acid, phenotypes correlated w
30 ne H4 acetylation, increased resistance to 6-azauracil, and cryptic transcription.
31 actor) are synthetically hypersensitive to 6-azauracil, and that deletions in the CTD reduce in vivo
32 e furanose ring but was substituted with a 6-azauracil base in place of uracil.
33 eatment with the nucleotide-depleting drug 6-azauracil exacerbated the effect preferentially in the m
34 -3 rpb2-101 double mutant was sensitive to 6-azauracil in vivo and to nucleoside triphosphate substra
35 st at RNA polymerase II pause sites due to 6-azauracil-induced nucleotide pool depletion was reduced
36 report that in organic medium (CDCl3), the 5-azauracil moiety forms hydrogen-bond-mediated complexes
37 o be consistent with the ionization of the 5-azauracil moiety in aqueous medium leading to competitiv
38 h dichotomous base-pairing behavior of the 5-azauracil moiety, in organic versus aqueous media, is fo
39 on unless cells are exposed to conditions (6-azauracil or reduced temperature) that are presumed to a
40 II (Pol II), we analyzed properties of the 6-azauracil-sensitive and TFIIS-dependent E1103G mutant of
41 vated slippage rates were identified among 6-azauracil-sensitive mutants and were also isolated using
42 olymerase II purified from three different 6-azauracil-sensitive yeast strains displayed increased ar
43 scription elongation defects as assayed by 6-azauracil sensitivity.
44 ferred sensitivity to growth inhibition by 6-azauracil that was exacerbated by partial truncations of