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1 inhibitors actinomycin D, DRB, H7 and alpha-amanitin.
2 inhibition of ongoing transcription by alpha-amanitin.
3 ranscription was globally inhibited by alpha-amanitin.
4 stant to the transcriptional inhibitor alpha-amanitin.
5 the effect with low concentrations of alpha-amanitin.
6 uming transcription in the presence of alpha-amanitin.
7 of transcription as it is resistant to alpha-amanitin.
8 tivity of stalled transcription complexes to amanitin.
9 polymerase II, the subunit that binds alpha-amanitin.
10 age in arrested complexes is not affected by amanitin.
11 on of endogenous Pol II using a toxin, alpha-amanitin.
12 as does inhibition of transcription by alpha-amanitin.
13 l chromatin insulators are affected by alpha-amanitin.
14 inished by treatment of the cells with alpha-amanitin.
15 ex, which is specifically inhibited by alpha-amanitin.
16 n active transcription and arrested by alpha-amanitin.
17 lectively resistant to inhibition with alpha-amanitin.
18 racts with the transcription inhibitor alpha-amanitin.
19 scription in Giardia is resistant to 1 mg/ml amanitin.
20 iptional inhibitors, actinomycin D and alpha-amanitin.
21 high concentrations (100 microg/ml) of alpha-amanitin.
22 D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin.
23 merase inhibitors on HDV genome replication: amanitin, 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazo
24 oding genes is relatively resistant to alpha-amanitin (50% inhibition = 250 microg alpha-amanitin/ml)
25 hat is resistant to the mushroom toxin alpha-amanitin, a characteristic of transcription by RNA pol I
26 riole overduplication are abrogated by alpha-amanitin, a potent and specific RNA pol II inhibitor.
27 pol II dephosphorylation confirmed by alpha-amanitin, a specific RNA pol II inihibitor, showing pote
28 presence of the translocation blocker alpha-amanitin, a steady state condition is established in whi
32 of Pol II is significantly induced by alpha-amanitin, an amatoxin that blocks Pol II elongation and
33 rigera, AMA1 and PHA1, directly encode alpha-amanitin, an amatoxin, and the related bicyclic heptapep
35 e II (RNAPII) translocation inhibitors alpha amanitin and 5,6-dichloro-1-beta-D-ribobenzimidazole (DR
36 hepatocytes were also observed in the alpha-amanitin and acetaminophen-induced liver injury mouse mo
37 e show that transcriptional inhibitors alpha-amanitin and actinomycin D specifically disrupt the symm
38 ion factor eIF-4C that is inhibited by alpha-amanitin and correlated with a transient increase in the
39 of G. lamblia RNAP II transcription to alpha-amanitin and found that unlike most other eukaryotes, RN
43 riptional inhibitors actinomycin D and alpha-amanitin and requires the kinase activity of ATM but not
44 manitin but sensitive to 100 microg/ml alpha-amanitin and tagetitoxin, suggesting involvement of RNA
45 e II that is relatively insensitive to alpha-amanitin and that differs from typical eukaryotic RNA po
46 uire an RNA primer, are insensitive to alpha-amanitin, and differ in their ability to displace the no
49 side triphosphate (NTP) substrates and alpha-amanitin are added to a human RNA polymerase II elongati
52 d to correlate with the sensitivity to alpha-amanitin, as S. pombe was intermediate between human and
57 ed by co-incubation with picrotoxin or alpha-amanitin but is insensitive to nifedipine, indicating th
58 tant to the RNA polymease II inhibitor alpha-amanitin but is sensitive to short interfering RNA speci
59 of TARE-6 was resistant to 1 microg/ml alpha-amanitin but sensitive to 100 microg/ml alpha-amanitin a
62 ized by an RNA polymerase resistant to alpha-amanitin, consistent with previously published reports r
65 gamma interferon or its inhibition by alpha-amanitin did not alter nucleosome occupancy, positioning
67 ase II in a complex with the inhibitor alpha-amanitin has been determined by x-ray crystallography.
70 icrograms/ml but not 1 microgram/ml of alpha-amanitin indicates transcription of the mouse YRNA genes
71 lly renders Pol II highly resistant to alpha-amanitin, indicating a functional interaction between Hi
72 tion of the GP63 genes is sensitive to alpha-amanitin, indicating that they are transcribed by a diff
73 ription of the ESAG-Is is sensitive to alpha-amanitin, indicating that they are transcribed by a diff
75 ir sensitivity to DRB, indicating that alpha-amanitin induces apoptosis solely by inhibiting RNAP II
78 s indicated that this apparent resistance to amanitin inhibition of genomic and antigenomic RNA relat
81 in the following bond addition cycle, alpha-amanitin inhibits elongation at each translocation step.
88 itivity to different concentrations of alpha-amanitin is that expected for human RNA polymerase III;
89 -beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 protein.
90 as inhibited by a low concentration of alpha-amanitin (<3 microgram/ml) and could be partially restor
93 presence of the translocation blocker alpha-amanitin, NTPs (but not deoxynucleotide triphosphate [dN
94 the effect of the fungus-derived toxin alpha-amanitin on the transcription of protein-coding genes of
97 ating Pol II-DNA complexes arrested by alpha-amanitin or cisplatin lesions, triggering ubiquitination
100 mplexes were slowed by the presence of alpha-amanitin, origin activity depended on the orientation of
103 Inhibition of Pol II activity using alpha-amanitin reduced expression of a number of Pol III genes
104 udy we carry out a genetic analysis of alpha-amanitin resistance in a population sample of Drosophila
105 pport previous proposals of the mechanism of amanitin resistance in other organisms and provide a mol
111 s contribute to the difference between alpha-amanitin-resistant and alpha-amanitin-sensitive third ch
112 and could be partially restored by an alpha-amanitin-resistant mutant pol II; however, surprisingly,
115 ing plasmid constructs that express an alpha-amanitin-resistant RNAP II subunit with a truncated or f
117 script cleavage activity which is completely amanitin-resistant; furthermore, pyrophosphorolytic tran
118 ts, and inhibition of transcription by alpha-amanitin resulted in the initiation of replication withi
119 ed with the transcriptional inhibitor, alpha-amanitin, revealed that the symmetry of cell division is
124 eChip set, we characterized the set of alpha-amanitin-sensitive genes expressed during the 1- and 2-c
125 e between alpha-amanitin-resistant and alpha-amanitin-sensitive third chromosome lines, the underlyin
126 0 intergenic region promoter can drive alpha-amanitin-sensitive transcription at an internal position
131 carried out by an RNA polymerase with alpha-amanitin sensitivity reminiscent of SL RNA synthesis and
132 nscription began, but experiments with alpha-amanitin show that cyclin E degradation is not dependent
133 e 50-amino-acid region thought to bind alpha-amanitin shows that this region of the trichomonad RNA p
135 t of cells with actinomycin D, DRB, or alpha-amanitin, specific inhibitors of Pol II, disperses ELL a
137 cription in CS-B cells is sensitive to alpha-amanitin, suggesting that it is RNA polymerase II-depend
138 llowing activation but is sensitive to alpha-amanitin, suggesting that polymerase movement is needed
139 ucleotides into RNA in the presence of alpha-amanitin, suggesting that the polymerase I enzyme is par
140 V RNAs have different sensitivities to alpha-amanitin, suggesting that these two strands are synthesi
141 polymerase inhibitors tagetitoxin and alpha-amanitin that are consistent with RNA polymerase II tran
142 tional interaction between His1085 and alpha-amanitin that is supported by rerefinement of an alpha-a
143 the two-cell stage in the presence of alpha-amanitin, this change in transcript abundance is not obs
144 b) antigenomic RNA was not affected by alpha-amanitin to a concentration higher than 25 microgram/ml.
146 ion capability could be tuned by conjugating amanitin to the C-terminus of pHLIP via linkers of diffe
148 bit RNA polymerases I, II, and III) or alpha-amanitin (to inhibit RNA polymerases II and III) as well
150 s outside the plant kingdom (e.g., the alpha-amanitin toxin gene family in the mushroom, Amanita bisp
151 chemical mutation' tools coupling with alpha-amanitin transcription inhibition assay to systematicall
154 gle- and triple-knockdown experiments, alpha-amanitin treatment, transcriptome profiling and chromati
156 Apoptosis induced by cycloheximide or alpha-amanitin was blocked by injection of RNA encoding Xenopu
158 by the POP of C. albipes, but a precursor of amanitin (which is not made by C. albipes) was cleaved i
161 D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin, which inhibit RNAP II function by two distinct
164 resistant to induction of apoptosis by alpha-amanitin without affecting their sensitivity to DRB, ind
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