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1 persensitivity to the anti-elongation drug 6-azauracil.
2 ene renders S. pombe sensitive to the drug 6-azauracil.
3 phenotypes and an increased sensitivity to 6-azauracil.
4 than wild type to the cytotoxic effect of 6-azauracil.
5 h sensitivity to growth in the presence of 6-azauracil.
6 s sensitive to growth on medium containing 6-azauracil.
7 increased H4 acetylation and resistance to 6-Azauracil.
8 adenine compounds, whereas derivatives of 5-azauracil (2,4-dioxotriazine) are known to form weak com
9 under 'transcriptional stress' induced by 6-azauracil (6-AU) and inactivation of pol II, TFIIE or CT
10 but snz1 and sno1 mutants are sensitive to 6-azauracil (6-AU), an inhibitor of purine and pyrimidine
12 s overexpression of the NOT4 gene elicited 6-azauracil (6AU) and mycophenolic acid sensitivities, hal
14 ne enzyme in vitro, confers sensitivity to 6-azauracil (6AU), a drug that depresses cellular nucleosi
15 sensitivity to a drug that inhibits IMPDH, 6-azauracil (6AU), by a mechanism that is poorly understoo
20 s in the Paf1 complex cause sensitivity to 6-azauracil and diminished PUR5 induction, properties freq
21 BUR1 mutants are sensitive to the drugs 6-azauracil and mycophenolic acid and interact genetically
23 itive to inhibitors of this enzyme such as 6-azauracil and mycophenolic acid, at least partly because
24 t a deletion of RTF1 causes sensitivity to 6-azauracil and mycophenolic acid, phenotypes correlated w
26 actor) are synthetically hypersensitive to 6-azauracil, and that deletions in the CTD reduce in vivo
28 eatment with the nucleotide-depleting drug 6-azauracil exacerbated the effect preferentially in the m
29 -3 rpb2-101 double mutant was sensitive to 6-azauracil in vivo and to nucleoside triphosphate substra
30 st at RNA polymerase II pause sites due to 6-azauracil-induced nucleotide pool depletion was reduced
31 report that in organic medium (CDCl3), the 5-azauracil moiety forms hydrogen-bond-mediated complexes
32 o be consistent with the ionization of the 5-azauracil moiety in aqueous medium leading to competitiv
33 h dichotomous base-pairing behavior of the 5-azauracil moiety, in organic versus aqueous media, is fo
34 on unless cells are exposed to conditions (6-azauracil or reduced temperature) that are presumed to a
35 II (Pol II), we analyzed properties of the 6-azauracil-sensitive and TFIIS-dependent E1103G mutant of
36 vated slippage rates were identified among 6-azauracil-sensitive mutants and were also isolated using
37 olymerase II purified from three different 6-azauracil-sensitive yeast strains displayed increased ar
39 ferred sensitivity to growth inhibition by 6-azauracil that was exacerbated by partial truncations of
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