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1 ial growth and low homology with other human topoisomerases.
2 ne interactions with other bacterial type II topoisomerases.
3 supercoiled DNA to nicking endonucleases and topoisomerases.
4 romoter and the temporal expression of three topoisomerases.
5 nalyzed three putative Chlamydia trachomatis topoisomerases.
6 d, most have not been tested with respect to topoisomerases.
7 o be regulated by a family of enzymes called topoisomerases.
8 mode-of-inhibition against bacterial type II topoisomerases.
9 he transcription machinery directly controls topoisomerase 1 (TOP1) activity to adjust DNA topology t
11 fied depletion of ATR as a top candidate for topoisomerase 1 (TOP1) inhibitor synthetic lethality and
13 ed proteins that function in RNA metabolism (Topoisomerase 1 and RNA helicases), DNA repair/replicati
17 encing (ChIP-seq) versus TOP1 activity using topoisomerase 1 sequencing (TOP1-seq), a method reported
18 RNA polymerase II is increased, and that of topoisomerase 1, an R-loop preventing factor, is decreas
21 osyl-DNA phosphodiesterase 2 (Tdp2) reverses Topoisomerase 2 (Top2) DNA-protein crosslinks triggered
24 ether with the downregulation of its target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, res
25 vant as Hat1-/- cells are hyper-sensitive to topoisomerase 2 inhibition suggesting that Hat1 is requi
28 echanistically, ARID1A deficiency results in topoisomerase 2A and cell cycle defects, which cause an
31 rt that D loops can also be disrupted by DNA topoisomerase 3 (Top3), and this disruption depends on T
32 gion sharing high homology with DDR proteins Topoisomerase 3alpha (TOP3alpha) and NEIL3 (Nei-like DNA
33 emonstrate that the mitochondrial isoform of topoisomerase 3alpha (Top3alpha) fulfills this function,
35 elicase, a type IB topoisomerase, a type IIA topoisomerase, a non-specific mitochondrial DNA binding
36 pendent DNA binding of a helicase, a type IB topoisomerase, a type IIA topoisomerase, a non-specific
37 have revealed unexpected roles of type I DNA topoisomerases, a subclass of these enzymes, in regulati
38 referentially occur in contexts that inhibit topoisomerase action ahead of the fork, including stable
39 sms, including intra-chromosomal compaction, topoisomerase action and Holliday junction resolvases, e
41 erichia coli DNA topoisomerase I has low RNA topoisomerase activity and that the R173A point mutation
45 benzimidazoles (3, 6, 7, 8) also inhibit RNA topoisomerase activity of E. coli DNA topoisomerase I.
47 f endogenous lesions may arise from aberrant topoisomerase activity or ribonucleotide incorporation i
48 only known topoisomerase that possesses RNA topoisomerase activity, binds mRNA translation machinery
50 ng studies of a 97 kDa fragment spanning the topoisomerase and 10 (HhH)2 domains reveal that the (HhH
52 It has been reported that the absence of Topoisomerase and RNase H activity in Escherichia coli o
53 the topological conversion catalysed by DNA topoisomerase and to study the DNA replication under top
54 antibacterials that kill cells by inhibiting topoisomerases and inducing double-stranded DNA breaks.
56 tegy that can be applied to study additional topoisomerases and their inhibitors in vitro and in vivo
58 s focused on the biological functions of DNA topoisomerases, and several findings have revealed unexp
63 These new findings highlight that type I topoisomerases are still interesting targets for drug di
65 le out interaction with DNA or inhibition of topoisomerase, both of which are common modes of action
71 opyran-based inhibitors of bacterial type II topoisomerases (DNA gyrase and topoisomerase IV) display
75 ndrial topoisomerase I (TOP1MT) is a type IB topoisomerase encoded in the nucleus of vertebrate cells
76 lass of antibiotics, which targets bacterial topoisomerases, fails to kill bacteria that have grown t
78 Our data suggest that Top3beta is the major topoisomerase for mRNAs, and requires both RNA binding a
81 inhibition of Neisseria gonorrhoeae type II topoisomerases gyrase and topoisomerase IV by AZD0914 (A
82 lysis of gyrase B of the beta subunit of DNA topoisomerase (gyrB), and 16S rRNA and subunit A of SecA
83 the latter requires the CTD, indicating that topoisomerases have developed distinct mechanisms during
86 These deletion events are dependent on DNA topoisomerase I (Top1) and are initiated by Top1 incisio
93 ow rapid recruitment, within minutes, of DNA topoisomerase I (TOP1) to a large cohort of AR-regulated
94 transcription-associated damage in yeast is Topoisomerase I (Top1), an enzyme that removes torsional
95 ver, in a RNase H2 knock-out yeast strain, a topoisomerase I (Top1)-dependent mutator effect develops
98 mary cellular target of YjhX was found to be topoisomerase I (TopA), inhibiting both DNA replication
100 nteraction between the C-terminal domains of topoisomerase I (TopoI-CTDs) and the beta' subunit of RN
101 In addition, the described ligand displayed topoisomerase I activity inhibition and self-fluorescenc
102 e of the protein-protein interaction between topoisomerase I and RNA polymerase during stress respons
104 a distinct mechanism of interaction between topoisomerase I and RNA polymerase in Mycobacterium tube
106 consistent with negative feedback control of topoisomerase I and topoisomerase IV expression, which i
107 PB1 alleles using DNA obtained from 318 anti-topoisomerase I antibody-positive patients and 561 healt
110 biomarkers such as carbonic anhydrase IX and topoisomerase I by immunohistochemistry show clear evide
113 features observed for MtTOP1 may allow these topoisomerase I enzymes to carry out physiological funct
114 in M. smegmatis competed with the endogenous topoisomerase I for protein-protein interactions with RN
115 cal probe, we find that Escherichia coli DNA topoisomerase I has low RNA topoisomerase activity and t
116 p3beta differs from that of Escherichia coli topoisomerase I in that the former but not the latter re
117 rDNA and clarifies a structural role of DNA topoisomerase I in the epigenetic regulation of rDNA, in
118 ction by either transcription termination or topoisomerase I inhibition has been shown to increase pa
119 ochondrial inhibitors, intracellular ROS, or topoisomerase I inhibition orchestrates an inflammatory
120 yl side chains display excellent E. coli DNA topoisomerase I inhibition properties with IC50 values <
121 n synthesized and their Escherichia coli DNA topoisomerase I inhibition, binding to B-DNA duplex, and
123 nd PRC2 exhibit synthetic sensitivity to the topoisomerase I inhibitor Camptothecin and accumulate ga
126 n the present studies, an indenoisoquinoline topoisomerase I inhibitor was conjugated to DUPA via a p
127 p synthesis of a series of clinically active topoisomerase I inhibitors such as NSC 314622, LMP-400,
131 mutations in ribonuclease H, senataxin, and topoisomerase I that resolve RNA-DNA hybrids lead to inc
133 NA re-ligation, diminishes the expression of topoisomerase I, and enhances the expression of inter al
140 of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et
141 establish the optimal nitrogen position for topoisomerase IB (Top1) enzyme poisoning activity and cy
145 ll available thaumarchaeal genomes contain a topoisomerase IB gene that defines a monophyletic group
147 ble-strand breaks (DSBs) induced by abortive topoisomerase II (TOP2) activity are a potential source
148 y.DNA double-strand breaks (DSBs) induced by topoisomerase II (TOP2) are rejoined by TDP2-dependent n
149 ng 5'-tyrosyl DNA adducts formed by abortive topoisomerase II (Top2) cleavage complexes to allow erro
152 specifically repairs DNA damages induced by topoisomerase II (Top2) poisons and causes resistance to
153 nd immature myeloid cells and transforms the topoisomerase II (TOP2) poisons etoposide and mitoxantro
154 Here, we investigated the processing of topoisomerase II (Top2)-DNA adducts induced by treatment
156 olecular target of resveratrol is eukaryotic topoisomerase II (topo II), an enzyme essential for chro
158 , chromosomes present high levels of de novo Topoisomerase II (TopoII)-dependent re-entanglements, an
159 ce to anaphase, suggesting the importance of topoisomerase II activity for proper chromosome condensa
160 icated that XWL-1-48 significantly inhibited topoisomerase II activity in a concentration-dependent m
162 nly used chemotherapeutic drug that inhibits topoisomerase II activity, thereby leading to genotoxici
163 l elongation-coupled DDR signalling involves topoisomerase II because inhibiting this enzyme interfer
165 d by new insights that anthracycline targets topoisomerase II beta to cause DNA double-strand breaks
167 pattern indicates the active requirement of topoisomerase II during these stages of the cell cycle.
170 cell cultures were used to study the role of topoisomerase II in various stages of the cell cycle.
176 he immuno-staining analysis also showed that topoisomerase II is the major component of mitotic chrom
177 r inter-sister homologous recombination, and topoisomerase II plays a role in generating the damage.
179 are selectively resistant to treatment with topoisomerase II poisons but not other DNA damaging agen
182 ty to 12% of the tested compounds, including topoisomerase II, B-cell chronic lymphocytic leukemia/ly
183 tinostat and doxorubicin treatment inhibited topoisomerase II-beta (TopoII-beta) and relieved TopoII-
184 s and found that NONO favours the loading of topoisomerase II-binding protein 1 acting upstream of th
186 riant CENP-A and the DNA decatenizing enzyme topoisomerase-II (topo-II) as candidate modulators of ch
188 sensitivity to anthracyclines by recruiting topoisomerase IIa (TOP2A) to DNA and increasing double-s
189 gg extract, we found that SUMOylation of DNA topoisomerase IIalpha (TOP2A) CTD regulates the localiza
193 ence that the C-terminal domain (CTD) of DNA topoisomerase IIalpha (Topo II) provides a novel functio
196 Interestingly, PICH also bound to SUMOylated topoisomerase IIalpha (TopoIIalpha), a major centromeric
197 chromosomes during meiosis, localization of topoisomerase IIalpha to bivalents was not affected; how
199 st proteins identified by mass spectrometry, topoisomerases IIalpha and IIbeta and PCNA were notewort
200 potential roles of host proteins, including topoisomerases IIalpha and IIbeta and PCNA, which were f
201 cted role for the cutting of promoter DNA by topoisomerase IIB to facilitate transcription of activit
202 es showed that Ku70/86 and components of the topoisomerase IIbeta (TOP2beta)/poly(ADP ribose) polymer
203 at Beclin 1 could directly interact with DNA topoisomerase IIbeta and was recruited to the DSB sites
204 (Top2) and one of its interacting partners, topoisomerase IIbeta binding protein 1 (TopBP1) are two
213 ain the synthetic lethality observed between topoisomerase-induced DNA breaks and the RecBCD gene pro
214 h its dual action as an alkylating agent and topoisomerase inhibitor, represents a novel anti-cancer
215 s that can repair damaged DNA resulting from topoisomerase inhibitors and a variety of other DNA-dama
216 mulin, a pleuromutilin, and new nonquinolone topoisomerase inhibitors are attractive possibilities th
219 ls more susceptible to cell death induced by topoisomerase inhibitors in an oncology drug screening a
221 lung cancer cells are largely insensitive to topoisomerase inhibitors, and depletion of PKCdelta can
222 -Ras-independent cells are more sensitive to topoisomerase inhibitors, and depletion of PKCdelta in t
223 antly, we demonstrate that DNA damage drugs, topoisomerase inhibitors, can trigger CKI activation to
225 cells to be more sensitive to type I and II topoisomerase inhibitors, Raf inhibitors, and other drug
234 ng sites located on bacterial DNA gyrase and topoisomerase IV and not utilized by marketed antibiotic
235 onorrhoeae type II topoisomerases gyrase and topoisomerase IV by AZD0914 (AZD0914 will be henceforth
238 caffold against the N-terminal domain of the topoisomerase IV E subunit from Escherichia coli (eParE)
239 ncodes a protein that does not interact with topoisomerase IV exhibit severe nucleoid decompaction le
240 tive feedback control of topoisomerase I and topoisomerase IV expression, which is typical of other b
243 ibition of the topoisomerases DNA gyrase and topoisomerase IV from both Gram-positive and a Gram-nega
244 ed with negatively supercoiled) DNA, whereas topoisomerase IV generated similar levels with both subs
246 ased optimization toward dual DNA gyrase and topoisomerase IV inhibitors with antibacterial activity.
250 us anthracis and Escherichia coli gyrase and topoisomerase IV to relax and cleave positively supercoi
251 s indicate that gyrase is better suited than topoisomerase IV to safely remove positive supercoils th
252 positive supercoiling behind the fork where topoisomerase IV would also act to maintain replicating
253 erial type II topoisomerases (DNA gyrase and topoisomerase IV) display potent activity against Gram-p
255 are potent inhibitors of both DNA gyrase and topoisomerase IV, displaying antibacterial activities ag
256 ulates intramolecular reactions catalyzed by topoisomerase IV, supercoiled DNA relaxation, and DNA kn
262 st DNA gyrase from Staphylococcus aureus and topoisomerases IV from E. coli and S. aureus were determ
263 eated by Spo11, the evolutionarily conserved topoisomerase-like protein, but how these DSBs are distr
264 ed Actinobacteria, this subfamily of type IA topoisomerase may be required for multiple functions in
265 ll, Canela et al. (2017) reveal that type II topoisomerase-mediated release of torsional strain at ch
266 of topological enzymes such as type I and II topoisomerase, most of these defects can be avoided and
267 104) or absence (n = 49) of gyrA and/or parC topoisomerase mutations, qnrA, qnrB, qnrD, qnrS, aac(6')
271 but not the final bicyclopentadione) mediate topoisomerase poisoning and possibly many other activiti
272 sublethal genotoxic treatments, using other topoisomerase poisons, DNA synthesis inhibitors, interst
277 o deficient in binding mRNAs, catalyzing RNA topoisomerase reaction, and promoting synapse formation.
278 s and the same catalytic residue used in DNA topoisomerase reaction; however, it does not absolutely
281 p1 proteins, a histone deacetylase and a DNA topoisomerase, respectively, we investigated whether gen
282 interactors-including cohesins, condensins, topoisomerases, RNA helicases, chromatin remodelers, and
284 Bacterial gyrases are a class of type II topoisomerases that can introduce negative supercoiling
285 he mechanism of genome regulation by type IA topoisomerases that is essential for life, as well as th
287 ed through transient DNA fracture by type II topoisomerases to permit chromosome segregation during c
297 more than one (HhH)2 domain, the only known topoisomerase with dual activities and is also unique by
299 d on cell and/or patient survival, including topoisomerases with RAD17 and checkpoint kinases with BL
300 model analogous to that observed for type IB topoisomerases, with religation probability varying in a
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