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 pological enzymes, such as type I or type II topoisomerases).
2 NA synthesis, even in the absence of type II topoisomerase.
3 isome components and both type I and type II topoisomerases.
4 es $(K,\Delta Lk)$ in DNA induced by type-II topoisomerases.
5 ficient to take over the function of type 1A topoisomerases.
6 torsional stress injected in the molecule by topoisomerases.
7 tify drug-resistance mutations in eukaryotic topoisomerases.
8 ription and hyperproliferation by activating topoisomerases.
10 fied depletion of ATR as a top candidate for topoisomerase 1 (TOP1) inhibitor synthetic lethality and
11 lidation of a quinoline-based novel class of topoisomerase 1 (Top1) inhibitors and establish that com
14 lently closed circle of double-stranded DNA, topoisomerase 1 (Topo1) is thought to be required for pr
17 sm to K-PPn of two yeast proteins, Top1 (DNA topoisomerase 1) and Nsr1 (nuclear signal recognition 1)
18 RNA polymerase II is increased, and that of topoisomerase 1, an R-loop preventing factor, is decreas
19 tically predicted immunodominant peptides of topoisomerase 1, fibrillarin, and centromere protein A a
20 d into DNA during replication are removed by Topoisomerase 1, which generates 3' terminal adducts tha
25 ether with the downregulation of its target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, res
26 osyl-DNA phosphodiesterase 2 (TDP2) reverses Topoisomerase 2 DNA-protein crosslinks (TOP2-DPCs) in a
27 phosphodiesterase activity removing stalled topoisomerase 2 from DNA, TDP2 has also been shown to in
28 vant as Hat1-/- cells are hyper-sensitive to topoisomerase 2 inhibition suggesting that Hat1 is requi
32 DNA double-strand breaks (DSBs) mediated by Topoisomerase 2beta-DNA cleavage complex (TOP2betacc) in
33 gion sharing high homology with DDR proteins Topoisomerase 3alpha (TOP3alpha) and NEIL3 (Nei-like DNA
35 have revealed unexpected roles of type I DNA topoisomerases, a subclass of these enzymes, in regulati
36 show how tight coupling of the helicase and topoisomerase activities allows for induction of positiv
39 benzimidazoles (3, 6, 7, 8) also inhibit RNA topoisomerase activity of E. coli DNA topoisomerase I.
40 f endogenous lesions may arise from aberrant topoisomerase activity or ribonucleotide incorporation i
41 only known topoisomerase that possesses RNA topoisomerase activity, binds mRNA translation machinery
45 Finally, we show that targeting R-loops with topoisomerase and PARP inhibitors might be an effective
46 nt-derived cell lines exhibit sensitivity to topoisomerase and PARP inhibitors, defective sister chro
47 It has been reported that the absence of Topoisomerase and RNase H activity in Escherichia coli o
49 ntial link between the catalytic activity of topoisomerases and the fundamental question regarding th
51 s focused on the biological functions of DNA topoisomerases, and several findings have revealed unexp
53 oisomerases, the many lives of these type IA topoisomerases are now being progressively revealed.
54 nance of cccDNA and reveal that cellular DNA topoisomerases are required for both de novo synthesis a
61 apping of prokaryotic and eukaryotic type II topoisomerases cleavage sites in a variety of organisms
64 opyran-based inhibitors of bacterial type II topoisomerases (DNA gyrase and topoisomerase IV) display
66 ve sweeps of mutations including the primary topoisomerase drug targets, whereas biofilm-adapted popu
67 ndrial topoisomerase I (TOP1MT) is a type IB topoisomerase encoded in the nucleus of vertebrate cells
69 poisomerase IB (TOP1MT) is a nuclear-encoded topoisomerase, exclusively localized to mitochondria, wh
70 lass of antibiotics, which targets bacterial topoisomerases, fails to kill bacteria that have grown t
73 Our data suggest that Top3beta is the major topoisomerase for mRNAs, and requires both RNA binding a
78 e-strand breaks (DSBs) in cells depleted for Topoisomerase I (Top1), an enzyme that relaxes DNA super
79 transcription-associated damage in yeast is Topoisomerase I (Top1), an enzyme that removes torsional
82 that mutations in the gene encoding for DNA topoisomerase I (topA) give rise to mutator phenotypes w
83 nteraction between the C-terminal domains of topoisomerase I (TopoI-CTDs) and the beta' subunit of RN
84 In addition, the described ligand displayed topoisomerase I activity inhibition and self-fluorescenc
86 ing this assay, we found that all the tested topoisomerase I and II (TOP1 and TOP2, respectively) poi
88 ations together, our study demonstrates that topoisomerase I and II may catalyze distinct steps of HB
89 e of the protein-protein interaction between topoisomerase I and RNA polymerase during stress respons
90 PB1 alleles using DNA obtained from 318 anti-topoisomerase I antibody-positive patients and 561 healt
91 NA binding domains to form diverse bacterial topoisomerase I enzymes that are highly efficient in the
92 in M. smegmatis competed with the endogenous topoisomerase I for protein-protein interactions with RN
94 n the essentiality of the topA gene encoding topoisomerase I in the model bacterium Bacillus subtilis
96 yl side chains display excellent E. coli DNA topoisomerase I inhibition properties with IC50 values <
97 n synthesized and their Escherichia coli DNA topoisomerase I inhibition, binding to B-DNA duplex, and
98 nt anticancer activity do not exhibit strong topoisomerase I inhibition, suggesting a separate mechan
99 h clinically-relevant nanomolar doses of the Topoisomerase I inhibitor camptothecin, loss of WRN exon
104 latform, the effect of an apoptotic inducer, topoisomerase I inhibitor, 7-ethyl-10-hydrocamptothecin
105 s synthesized by conjugating camptothecin, a topoisomerase I inhibitor, to our proprietary, 'clickabl
107 p synthesis of a series of clinically active topoisomerase I inhibitors such as NSC 314622, LMP-400,
110 amage induced by chemotherapy drugs, such as topoisomerase I inhibitors, results in S and G2 phase ar
112 tudy suggests that dual targeting of MYC and topoisomerase I may serve as a novel strategy for antica
114 oligonucleotides to Mycobacterium smegmatis topoisomerase I with progressive C-terminal deletions sh
116 DNA ends, like camptothecin-induced trapped-topoisomerase I, can be mediated by TDP1, BRCA1, CtIP an
117 l linkers, selective inhibitors of bacterial topoisomerase I, have been evaluated using bacterial cyt
118 topoisomerase II is both structurally (e.g., topoisomerase I, Hsp90, and kinases) and functionally (e
119 analogues for their MYC-inhibitory activity, topoisomerase I-inhibitory activity, and anticancer acti
120 in vivo evaluation of the combination of DNA topoisomerase I-targeted drugs and mTOR kinase inhibitor
124 nitially hypersensitive to the inhibition of topoisomerase I/II and PARP, but acquire drug resistance
126 of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et
129 y.DNA double-strand breaks (DSBs) induced by topoisomerase II (TOP2) are rejoined by TDP2-dependent n
134 n as a DUB inhibitor, PR-619 is a potent DNA topoisomerase II (TOP2) poison, inducing both DNA topois
137 that anthracyclines and mitoxantrone act as topoisomerase II (TOP2) poisons at low concentration but
138 how that the therapeutic cytotoxicity of DNA topoisomerase II (TOP2) poisons can be enhanced through
139 nd immature myeloid cells and transforms the topoisomerase II (TOP2) poisons etoposide and mitoxantro
145 (AML) inhibit the activity of the mammalian topoisomerase II (topo II) isoforms, topo II alpha and t
146 olecular target of resveratrol is eukaryotic topoisomerase II (topo II), an enzyme essential for chro
147 We previously reported a first set of hybrid topoisomerase II (topoII) poisons whose chemical core me
148 roquinazoline derivatives that inhibit human topoisomerase II (topoII), a validated target of antican
149 , chromosomes present high levels of de novo Topoisomerase II (TopoII)-dependent re-entanglements, an
150 ce to anaphase, suggesting the importance of topoisomerase II activity for proper chromosome condensa
151 icated that XWL-1-48 significantly inhibited topoisomerase II activity in a concentration-dependent m
155 ring together with Treslin/TICRR and TopBP1 (Topoisomerase II binding protein 1 (TopBP1)-interacting
157 ing resistance to poisons of human and yeast topoisomerase II derive from a rich mutational 'landscap
158 1 and TOP2, respectively) poisons as well as topoisomerase II DNA binding and ATPase inhibitors signi
159 pattern indicates the active requirement of topoisomerase II during these stages of the cell cycle.
162 cell cultures were used to study the role of topoisomerase II in various stages of the cell cycle.
163 for the adaptive response that bypasses the topoisomerase II inhibition----mediated G(2) arrest.
164 Mice were treated with vehicle, M3814 alone, topoisomerase II inhibitor alone, and M3814 in combinati
165 hibitor alone, and M3814 in combination with topoisomerase II inhibitor, and change in tumor volume o
167 e cellular ultrastructure that differed from topoisomerase II inhibitors including induction of spher
168 cancer therapy with radiation, platinum and topoisomerase II inhibitors preferentially selects for m
169 tivity of M3814 in combination with multiple topoisomerase II inhibitors, doxorubicin, etoposide, and
172 ual-target or multiple-target inhibitors, as topoisomerase II is both structurally (e.g., topoisomera
176 he immuno-staining analysis also showed that topoisomerase II is the major component of mitotic chrom
181 are selectively resistant to treatment with topoisomerase II poisons but not other DNA damaging agen
182 n the absence of cohesion, but inhibition of topoisomerase II prevents their resolution in anaphase.
184 , small interfering RNA (siRNA) knockdown of topoisomerase II significantly reduced cccDNA amplificat
185 s the scientific background behind targeting topoisomerase II together with a number of other targets
188 ty to 12% of the tested compounds, including topoisomerase II, B-cell chronic lymphocytic leukemia/ly
189 te the clinical success of drugs that target topoisomerase II, the development of resistant cancer ce
190 els of random strand passage, for example by topoisomerase II, would result in entanglements, increas
195 se anthracyclines work in part by inhibiting topoisomerase-II (TOP2) on accessible DNA(3,4), we hypot
196 riant CENP-A and the DNA decatenizing enzyme topoisomerase-II (topo-II) as candidate modulators of ch
198 somerase II (TOP2) poison, inducing both DNA topoisomerase IIalpha (TOP2A) and DNA topoisomerase IIbe
202 PICH function is apparent toward SUMOylated topoisomerase IIalpha (TopoIIalpha) after inhibition of
205 cate that miR-9-3p and miR-9-5p decrease DNA topoisomerase IIalpha protein 170 kDa expression levels
206 chromosomes during meiosis, localization of topoisomerase IIalpha to bivalents was not affected; how
208 potential roles of host proteins, including topoisomerases IIalpha and IIbeta and PCNA, which were f
209 is the first to demonstrate the presence of topoisomerase IIbeta (TOP2B) as the only TOP2 isoform in
210 th DNA topoisomerase IIalpha (TOP2A) and DNA topoisomerase IIbeta (TOP2B) covalent DNA complexes with
211 pathway, STAT-5 increases expression of the topoisomerase IIbeta-binding protein 1 (TopBP1), a scaff
215 e 3beta (Top3beta) is the only dual-activity topoisomerase in animals that can change topology for bo
216 e ribosome, penicillin-binding proteins, and topoisomerases in a pharmacologically relevant phenotypi
217 increased, demonstrating the involvement of topoisomerases in DSB generation at the pausing sites.
218 thways of topology simplification by type-II topoisomerases in terms of stationary probability distri
221 mic distribution and mechanisms underpinning topoisomerase-induced DNA breaks, we map Top2 DNA cleava
223 One of them is microcin B17, a bacterial topoisomerase inhibitor whose activity depends on the co
224 the toxicity of a parenterally administered topoisomerase inhibitor, it enhanced the activity of dox
226 of triple-negative breast cancer cells with topoisomerase inhibitors activates DNA damage response p
227 mulin, a pleuromutilin, and new nonquinolone topoisomerase inhibitors are attractive possibilities th
228 of small-molecule inhibitors, we identified topoisomerase inhibitors as a class of drugs that enhanc
230 enetically engineered oncolytic reovirus and topoisomerase inhibitors may provide a potent therapeuti
231 ated by forward genetics in combination with topoisomerase inhibitors more efficiently infect and kil
236 lung cancer cells are largely insensitive to topoisomerase inhibitors, and depletion of PKCdelta can
237 -Ras-independent cells are more sensitive to topoisomerase inhibitors, and depletion of PKCdelta in t
238 such as fluoroquinolones and novel bacterial topoisomerase inhibitors, can trap DNA cleavage complexe
239 ic semiconductors from deoxyribonucleic acid topoisomerase inhibitors, featuring conjugated backbone
244 , the release of torsional strain by type II topoisomerases is critical for converging replisomes to
245 discrimination by prokaryotic and eukaryotic topoisomerases is vital to therapeutic utility, but is p
246 hen gyrase, the sole T. thermophilus type II topoisomerase, is inhibited, TtAgo allows the bacterium
247 get proteins-2 in DNA gyrase (GyrA) and 1 in topoisomerase IV (ParC), which occur in a stepwise manne
249 by 34, that inhibit bacterial DNA gyrase and topoisomerase IV and display potent activity against cip
251 ncodes a protein that does not interact with topoisomerase IV exhibit severe nucleoid decompaction le
252 ed with negatively supercoiled) DNA, whereas topoisomerase IV generated similar levels with both subs
258 estigating the well-validated DNA gyrase and topoisomerase IV targets while preventing cross-resistan
259 us anthracis and Escherichia coli gyrase and topoisomerase IV to relax and cleave positively supercoi
260 s indicate that gyrase is better suited than topoisomerase IV to safely remove positive supercoils th
262 erial type II topoisomerases (DNA gyrase and topoisomerase IV) display potent activity against Gram-p
263 ulates intramolecular reactions catalyzed by topoisomerase IV, supercoiled DNA relaxation, and DNA kn
264 the classical quinolone binding site in the topoisomerase IV-DNA cleavage complex but does not form
267 ll, Canela et al. (2017) reveal that type II topoisomerase-mediated release of torsional strain at ch
268 creasing the fitness benefit provided by DNA topoisomerase mutations under ciprofloxacin treatment.
269 such as helicases, DNA and RNA polymerases, topoisomerases, nucleosome remodelers, and motors involv
272 nding and cleavage region of human and yeast topoisomerases (particularly hTOP2beta) is additionally
275 ential mechanism of developing resistance to topoisomerase poisons by ensuring rapid TOP2cc reversal.
277 is, and at telomeres as well as from aborted topoisomerase reactions, collapsed replication forks, an
278 n during viral DNA replication by regulating topoisomerase recruitment to the replication origin.IMPO
280 sing of a 50-nt non-coding gap in a phage T4 topoisomerase subunit gene (gp60) requires several recod
282 DP1 inhibitors is proposed to synergize with topoisomerase targeting drugs to enhance selectivity aga
285 Once thought to be the most unremarkable of topoisomerases, the many lives of these type IA topoisom
286 ed through transient DNA fracture by type II topoisomerases to permit chromosome segregation during c
289 A-phosphodiesterase I (TDP1) repairs type IB topoisomerase (TOP1) cleavage complexes generated by TOP
291 nscription factors Tcf4 and Tbr1 and the RNA topoisomerase Top3b shared a neuronal phenotype marked b
295 ne molecule is dispensable for the repair of topoisomerase type II (Top II) DNA adducts and associate
296 the description of a new class of bacterial topoisomerase type II inhibitors known as "novel bacteri
299 port here the crystal structure of a type IA topoisomerase with ssDNA segments bound in opposite pola