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1 bolish the effect with low concentrations of alpha-amanitin.
2 of resuming transcription in the presence of alpha-amanitin.
3 ndent of transcription as it is resistant to alpha-amanitin.
4 of RNA polymerase II, the subunit that binds alpha-amanitin.
5 radation of endogenous Pol II using a toxin, alpha-amanitin.
6 lity, as does inhibition of transcription by alpha-amanitin.
7 ctional chromatin insulators are affected by alpha-amanitin.
8 ly diminished by treatment of the cells with alpha-amanitin.
9 complex, which is specifically inhibited by alpha-amanitin.
10 aged in active transcription and arrested by alpha-amanitin.
11 is selectively resistant to inhibition with alpha-amanitin.
12 ar extracts with the transcription inhibitor alpha-amanitin.
13 ranscriptional inhibitors, actinomycin D and alpha-amanitin.
14 nt to high concentrations (100 microg/ml) of alpha-amanitin.
15 -beta-D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin.
16 thesis inhibitors actinomycin D, DRB, H7 and alpha-amanitin.
17 with inhibition of ongoing transcription by alpha-amanitin.
18 e II transcription was globally inhibited by alpha-amanitin.
19 s resistant to the transcriptional inhibitor alpha-amanitin.
20 tein-coding genes is relatively resistant to alpha-amanitin (50% inhibition = 250 microg alpha-amanit
21 rase that is resistant to the mushroom toxin alpha-amanitin, a characteristic of transcription by RNA
22 d centriole overduplication are abrogated by alpha-amanitin, a potent and specific RNA pol II inhibit
23 of RNA pol II dephosphorylation confirmed by alpha-amanitin, a specific RNA pol II inihibitor, showin
24 In the presence of the translocation blocker alpha-amanitin, a steady state condition is established
27 nation of Pol II is significantly induced by alpha-amanitin, an amatoxin that blocks Pol II elongatio
28 bisporigera, AMA1 and PHA1, directly encode alpha-amanitin, an amatoxin, and the related bicyclic he
30 ymerase II (RNAPII) translocation inhibitors alpha amanitin and 5,6-dichloro-1-beta-D-ribobenzimidazo
31 ptotic hepatocytes were also observed in the alpha-amanitin and acetaminophen-induced liver injury mo
32 We here show that transcriptional inhibitors alpha-amanitin and actinomycin D specifically disrupt th
33 nitiation factor eIF-4C that is inhibited by alpha-amanitin and correlated with a transient increase
34 ivity of G. lamblia RNAP II transcription to alpha-amanitin and found that unlike most other eukaryot
38 transcriptional inhibitors actinomycin D and alpha-amanitin and requires the kinase activity of ATM b
39 lpha-amanitin but sensitive to 100 microg/ml alpha-amanitin and tagetitoxin, suggesting involvement o
40 ymerase II that is relatively insensitive to alpha-amanitin and that differs from typical eukaryotic
41 V require an RNA primer, are insensitive to alpha-amanitin, and differ in their ability to displace
44 nucleoside triphosphate (NTP) substrates and alpha-amanitin are added to a human RNA polymerase II el
46 s found to correlate with the sensitivity to alpha-amanitin, as S. pombe was intermediate between hum
47 of genomic HDV RNA was totally inhibited by alpha-amanitin at concentrations as low as 2.5 microg/ml
49 blocked by co-incubation with picrotoxin or alpha-amanitin but is insensitive to nifedipine, indicat
50 resistant to the RNA polymease II inhibitor alpha-amanitin but is sensitive to short interfering RNA
51 ption of TARE-6 was resistant to 1 microg/ml alpha-amanitin but sensitive to 100 microg/ml alpha-aman
53 ynthesized by an RNA polymerase resistant to alpha-amanitin, consistent with previously published rep
54 ion by gamma interferon or its inhibition by alpha-amanitin did not alter nucleosome occupancy, posit
55 ition of pol I by cycloheximide or pol II by alpha-amanitin did not significantly affect the PNC.
56 olymerase II in a complex with the inhibitor alpha-amanitin has been determined by x-ray crystallogra
59 200 micrograms/ml but not 1 microgram/ml of alpha-amanitin indicates transcription of the mouse YRNA
60 cifically renders Pol II highly resistant to alpha-amanitin, indicating a functional interaction betw
61 nscription of the GP63 genes is sensitive to alpha-amanitin, indicating that they are transcribed by
62 Transcription of the ESAG-Is is sensitive to alpha-amanitin, indicating that they are transcribed by
64 ng their sensitivity to DRB, indicating that alpha-amanitin induces apoptosis solely by inhibiting RN
68 active in the following bond addition cycle, alpha-amanitin inhibits elongation at each translocation
74 e sensitivity to different concentrations of alpha-amanitin is that expected for human RNA polymerase
75 loro-1-beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 pro
76 tion was inhibited by a low concentration of alpha-amanitin (<3 microgram/ml) and could be partially
78 in the presence of the translocation blocker alpha-amanitin, NTPs (but not deoxynucleotide triphospha
79 yzing the effect of the fungus-derived toxin alpha-amanitin on the transcription of protein-coding ge
82 elongating Pol II-DNA complexes arrested by alpha-amanitin or cisplatin lesions, triggering ubiquiti
85 ion complexes were slowed by the presence of alpha-amanitin, origin activity depended on the orientat
89 his study we carry out a genetic analysis of alpha-amanitin resistance in a population sample of Dros
93 mutants contribute to the difference between alpha-amanitin-resistant and alpha-amanitin-sensitive th
94 am/ml) and could be partially restored by an alpha-amanitin-resistant mutant pol II; however, surpris
97 Using plasmid constructs that express an alpha-amanitin-resistant RNAP II subunit with a truncate
98 d human immunodeficiency virus 1, we used an alpha-amanitin-resistant system developed previously.
99 on units, and inhibition of transcription by alpha-amanitin resulted in the initiation of replication
100 injected with the transcriptional inhibitor, alpha-amanitin, revealed that the symmetry of cell divis
103 nd confirmed that HDV RNA synthesis had both alpha-amanitin-sensitive and -resistant components.
105 se GeneChip set, we characterized the set of alpha-amanitin-sensitive genes expressed during the 1- a
106 ference between alpha-amanitin-resistant and alpha-amanitin-sensitive third chromosome lines, the und
107 e hsp70 intergenic region promoter can drive alpha-amanitin-sensitive transcription at an internal po
112 ion is carried out by an RNA polymerase with alpha-amanitin sensitivity reminiscent of SL RNA synthes
113 ic transcription began, but experiments with alpha-amanitin show that cyclin E degradation is not dep
114 of the 50-amino-acid region thought to bind alpha-amanitin shows that this region of the trichomonad
115 eatment of cells with actinomycin D, DRB, or alpha-amanitin, specific inhibitors of Pol II, disperses
116 e show that inhibition of RNAPII activity by alpha-amanitin specifically blocks processing of rRNA.
117 Transcription in CS-B cells is sensitive to alpha-amanitin, suggesting that it is RNA polymerase II-
118 urs following activation but is sensitive to alpha-amanitin, suggesting that polymerase movement is n
119 ribonucleotides into RNA in the presence of alpha-amanitin, suggesting that the polymerase I enzyme
120 and HDV RNAs have different sensitivities to alpha-amanitin, suggesting that these two strands are sy
121 he RNA polymerase inhibitors tagetitoxin and alpha-amanitin that are consistent with RNA polymerase I
122 a functional interaction between His1085 and alpha-amanitin that is supported by rerefinement of an a
123 red to the two-cell stage in the presence of alpha-amanitin, this change in transcript abundance is n
124 (1.7-kb) antigenomic RNA was not affected by alpha-amanitin to a concentration higher than 25 microgr
127 o inhibit RNA polymerases I, II, and III) or alpha-amanitin (to inhibit RNA polymerases II and III) a
128 eptides outside the plant kingdom (e.g., the alpha-amanitin toxin gene family in the mushroom, Amanit
129 s as 'chemical mutation' tools coupling with alpha-amanitin transcription inhibition assay to systema
132 ly single- and triple-knockdown experiments, alpha-amanitin treatment, transcriptome profiling and ch
136 -beta-D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin, which inhibit RNAP II function by two di
139 cells resistant to induction of apoptosis by alpha-amanitin without affecting their sensitivity to DR
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