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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 s resistant to the inhibitors rifampicin and alpha-amanitin.
6 lity, as does inhibition of transcription by alpha-amanitin.
7 radation of endogenous Pol II using a toxin, alpha-amanitin.
8 ctional chromatin insulators are affected by alpha-amanitin.
9 ly diminished by treatment of the cells with 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  complex, which is specifically inhibited by alpha-amanitin.
14 ranscriptional inhibitors, actinomycin D and alpha-amanitin.
15 nt to high concentrations (100 microg/ml) of alpha-amanitin.
16 -beta-D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin.
17 thesis inhibitors actinomycin D, DRB, H7 and alpha-amanitin.
18  with inhibition of ongoing transcription by alpha-amanitin.
19 e II transcription was globally inhibited by alpha-amanitin.
20 s resistant to the transcriptional inhibitor alpha-amanitin.
21 tein-coding genes is relatively resistant to alpha-amanitin (50% inhibition = 250 microg alpha-amanit
22 rase that is resistant to the mushroom toxin alpha-amanitin, a characteristic of transcription by RNA
23 d centriole overduplication are abrogated by alpha-amanitin, a potent and specific RNA pol II inhibit
24 of RNA pol II dephosphorylation confirmed by alpha-amanitin, a specific RNA pol II inihibitor, showin
25 In the presence of the translocation blocker alpha-amanitin, a steady state condition is established
26                                              alpha-Amanitin, a transcription inhibitor, did not suppr
27     Inhibition of zygotic transcription with alpha-amanitin also induced apoptosis.
28 nation of Pol II is significantly induced by alpha-amanitin, an amatoxin that blocks Pol II elongatio
29  bisporigera, AMA1 and PHA1, directly encode alpha-amanitin, an amatoxin, and the related bicyclic he
30  delivery of a polar cell-impermeable toxin, alpha-amanitin, an inhibitor of RNA polymerase II.
31 ymerase II (RNAPII) translocation inhibitors alpha amanitin and 5,6-dichloro-1-beta-D-ribobenzimidazo
32 ptotic hepatocytes were also observed in the alpha-amanitin and acetaminophen-induced liver injury mo
33 We here show that transcriptional inhibitors alpha-amanitin and actinomycin D specifically disrupt th
34 nitiation factor eIF-4C that is inhibited by alpha-amanitin and correlated with a transient increase
35 ivity of G. lamblia RNAP II transcription to alpha-amanitin and found that unlike most other eukaryot
36 as compared with 8-cell embryos treated with alpha-amanitin and MII.
37                      In Amanita bisporigera, alpha-amanitin and phallacidin are synthesized as 35- an
38                                              alpha-Amanitin and phallacidin are synthesized as propro
39 transcriptional inhibitors actinomycin D and alpha-amanitin and requires the kinase activity of ATM b
40 lpha-amanitin but sensitive to 100 microg/ml alpha-amanitin and tagetitoxin, suggesting involvement o
41 ymerase II that is relatively insensitive to alpha-amanitin and that differs from typical eukaryotic
42  V require an RNA primer, are insensitive to alpha-amanitin, and differ in their ability to displace
43 NA-dependent RNA polymerases (actinomycin D, alpha-amanitin, and rifampin).
44 eta colocalized with RNA polymerase II in an alpha-amanitin- and actinomycin D-sensitive manner.
45 nucleoside triphosphate (NTP) substrates and alpha-amanitin are added to a human RNA polymerase II el
46                                        Using alpha-amanitin as a dynamic probe of the RNA polymerase
47 s found to correlate with the sensitivity to alpha-amanitin, as S. pombe was intermediate between hum
48  of genomic HDV RNA was totally inhibited by alpha-amanitin at concentrations as low as 2.5 microg/ml
49                       However, we found that alpha-amanitin-based antibody-drug conjugates are highly
50  blocked by co-incubation with picrotoxin or alpha-amanitin but is insensitive to nifedipine, indicat
51  resistant to the RNA polymease II inhibitor alpha-amanitin but is sensitive to short interfering RNA
52 ption of TARE-6 was resistant to 1 microg/ml alpha-amanitin but sensitive to 100 microg/ml alpha-aman
53               Here we show that low doses of alpha-amanitin-conjugated anti-epithelial cell adhesion
54 ynthesized by an RNA polymerase resistant to alpha-amanitin, consistent with previously published rep
55 ion by gamma interferon or its inhibition by alpha-amanitin did not alter nucleosome occupancy, posit
56 ition of pol I by cycloheximide or pol II by alpha-amanitin did not significantly affect the PNC.
57 olymerase II in a complex with the inhibitor alpha-amanitin has been determined by x-ray crystallogra
58            Previous clinical applications of alpha-amanitin have been limited owing to its liver toxi
59                  Transcription inhibition by alpha-amanitin in vitro enhanced pol II ubiquitylation a
60  200 micrograms/ml but not 1 microgram/ml of alpha-amanitin indicates transcription of the mouse YRNA
61 cifically renders Pol II highly resistant to alpha-amanitin, indicating a functional interaction betw
62 nscription of the GP63 genes is sensitive to alpha-amanitin, indicating that they are transcribed by
63 Transcription of the ESAG-Is is sensitive to alpha-amanitin, indicating that they are transcribed by
64 as unaffected by either kinase inhibitors or alpha-amanitin-induced depletion of pol II.
65 ng their sensitivity to DRB, indicating that alpha-amanitin induces apoptosis solely by inhibiting RN
66         Additionally, both actinomycin D and alpha-amanitin inhibited the increase in uPA mRNA by PAF
67                              We propose that alpha-amanitin-inhibited Pol II elongation, which is slo
68                                   We show by alpha-amanitin inhibition that RNA polymerase II (RNAPII
69 active in the following bond addition cycle, alpha-amanitin inhibits elongation at each translocation
70                                              alpha-Amanitin insensitivity confirmed that overexpressi
71 d substrate selectivity, results from direct alpha-amanitin interference with the TL.
72                                     Although alpha-amanitin interferes with the transcript cleavage s
73               We show that pHLIP can deliver alpha-amanitin into cells in a pH-dependent fashion and
74                                    The toxin alpha-amanitin is frequently employed to completely bloc
75 e sensitivity to different concentrations of alpha-amanitin is that expected for human RNA polymerase
76 loro-1-beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 pro
77 tion was inhibited by a low concentration of alpha-amanitin (<3 microgram/ml) and could be partially
78  alpha-amanitin (50% inhibition = 250 microg alpha-amanitin/ml).
79 in the presence of the translocation blocker alpha-amanitin, NTPs (but not deoxynucleotide triphospha
80 yzing the effect of the fungus-derived toxin alpha-amanitin on the transcription of protein-coding ge
81                      Treatment of cells with alpha-amanitin or actinomycin D revealed that extension
82 ect was blocked by cycloheximide, but not by alpha-amanitin or actinomycin D.
83  elongating Pol II-DNA complexes arrested by alpha-amanitin or cisplatin lesions, triggering ubiquiti
84                   Suppression of POLR2A with alpha-amanitin or small interfering RNAs selectively inh
85            Inhibition of transcription using alpha-amanitin, or the dissolution of R loops by transie
86 ion complexes were slowed by the presence of alpha-amanitin, origin activity depended on the orientat
87 vating model and models of acetaminophen and alpha-amanitin poisoning were used.
88 itin that is supported by rerefinement of an alpha-amanitin-Pol II crystal structure.
89          Inhibition of Pol II activity using alpha-amanitin reduced expression of a number of Pol III
90 his study we carry out a genetic analysis of alpha-amanitin resistance in a population sample of Dros
91                  Engineered expression of an alpha-amanitin resistance RNAP II gene rendered cells re
92 m in a multidrug resistance gene (Mdr65A) in alpha-amanitin resistance.
93             The antigenomic RNA labeling was alpha-amanitin resistant and localized to the nucleolus.
94 mutants contribute to the difference between alpha-amanitin-resistant and alpha-amanitin-sensitive th
95 am/ml) and could be partially restored by an alpha-amanitin-resistant mutant pol II; however, surpris
96                                     Using an alpha-amanitin-resistant polymerase, we provide evidence
97                                    Utilizing alpha-amanitin-resistant RNA polymerase II mutants with
98     Using plasmid constructs that express an alpha-amanitin-resistant RNAP II subunit with a truncate
99 d human immunodeficiency virus 1, we used an alpha-amanitin-resistant system developed previously.
100 on units, and inhibition of transcription by alpha-amanitin resulted in the initiation of replication
101 injected with the transcriptional inhibitor, alpha-amanitin, revealed that the symmetry of cell divis
102                 The genomic RNA labeling was alpha-amanitin sensitive and more diffusely localized in
103 the 4.3 and 4.4 loci) whose transcription is alpha-amanitin sensitive.
104 nd confirmed that HDV RNA synthesis had both alpha-amanitin-sensitive and -resistant components.
105                                     Based on alpha-amanitin-sensitive BrUTP incorporation, transcript
106 se GeneChip set, we characterized the set of alpha-amanitin-sensitive genes expressed during the 1- a
107 ference between alpha-amanitin-resistant and alpha-amanitin-sensitive third chromosome lines, the und
108 e hsp70 intergenic region promoter can drive alpha-amanitin-sensitive transcription at an internal po
109  tsp, was functionally sufficient to support alpha-amanitin-sensitive transcription.
110 pts present on the MOE430 GeneChip set to be alpha-amanitin-sensitive.
111  of genes expressed in the 2-cell embryo are alpha-amanitin-sensitive.
112                          A comparison of the alpha-amanitin sensitivity of transcription in naturally
113 ion is carried out by an RNA polymerase with alpha-amanitin sensitivity reminiscent of SL RNA synthes
114 ic transcription began, but experiments with alpha-amanitin show that cyclin E degradation is not dep
115  of the 50-amino-acid region thought to bind alpha-amanitin shows that this region of the trichomonad
116 eatment of cells with actinomycin D, DRB, or alpha-amanitin, specific inhibitors of Pol II, disperses
117 e show that inhibition of RNAPII activity by alpha-amanitin specifically blocks processing of rRNA.
118  Transcription in CS-B cells is sensitive to alpha-amanitin, suggesting that it is RNA polymerase II-
119 urs following activation but is sensitive to alpha-amanitin, suggesting that polymerase movement is n
120  ribonucleotides into RNA in the presence of alpha-amanitin, suggesting that the polymerase I enzyme
121 and HDV RNAs have different sensitivities to alpha-amanitin, suggesting that these two strands are sy
122 he RNA polymerase inhibitors tagetitoxin and alpha-amanitin that are consistent with RNA polymerase I
123 a functional interaction between His1085 and alpha-amanitin that is supported by rerefinement of an a
124                                For 70 years, alpha-amanitin, the most cytotoxic peptide in its class,
125 red to the two-cell stage in the presence of alpha-amanitin, this change in transcript abundance is n
126 (1.7-kb) antigenomic RNA was not affected by alpha-amanitin to a concentration higher than 25 microgr
127 nous insulin receptors in cells treated with alpha-amanitin to block host cell mRNA synthesis.
128                            When treated with alpha-amanitin to inhibit transcription or JQ-1 to inhib
129 istribution described nonspecific binding of alpha-amanitin to yeast RNA polymerase II.
130 o inhibit RNA polymerases I, II, and III) or alpha-amanitin (to inhibit RNA polymerases II and III) a
131 eptides outside the plant kingdom (e.g., the alpha-amanitin toxin gene family in the mushroom, Amanit
132 s as 'chemical mutation' tools coupling with alpha-amanitin transcription inhibition assay to systema
133 ntriole duplication proceeded undisturbed in alpha-amanitin-treated cells.
134                                              alpha-Amanitin treatment had no effect on the ratio of p
135 ly single- and triple-knockdown experiments, alpha-amanitin treatment, transcriptome profiling and ch
136        Apoptosis induced by cycloheximide or alpha-amanitin was blocked by injection of RNA encoding
137                     Following treatment with alpha amanitin we observed a profound reduction in the o
138 y isoleucine (DHIle), an amino acid found in alpha-amanitin, which appears to be critical for toxicit
139                              The addition of alpha-amanitin, which can inhibit transcription, reduced
140 -beta-D-ribofuranosylbenzimidazole (DRB) and alpha-amanitin, which inhibit RNAP II function by two di
141              We find that the mushroom toxin alpha-amanitin, which inhibits TL mobility, suppresses t
142          Embryos cultured in the presence of alpha-amanitin, which permitted the distinguishing of ma
143                         PADT is inhibited by alpha-amanitin, which presumably blocks the required con
144 cells resistant to induction of apoptosis by alpha-amanitin without affecting their sensitivity to DR

 
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