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1 ds be referred to as 'topological poisons of topoisomerase I'.
2 TATA-dependent transcription such as NC2 and Topoisomerase I.
3 induction by the covalent complex formed by topoisomerase I.
4 or by the formation of poly(ADP-ribosyl)ated topoisomerase I.
5 wn previously to act as poisons of human DNA topoisomerase I.
6 s negative DNA supercoils in the presence of topoisomerase I.
7 of ARF/topoisomerase I complex and DNA-bound topoisomerase I.
8 it RNA topoisomerase activity of E. coli DNA topoisomerase I.
9 in and amino acids of the active site of DNA topoisomerase I.
10 o subunits of DNA gyrase, whereas CT643 is a topoisomerase I.
11 n the C-terminal domains of Escherichia coli topoisomerase I.
12 st endogenous protein inhibitor specific for topoisomerase I.
15 P and other nucleotides in the regulation of topoisomerase I activity in the presence of camptothecin
16 In addition, the described ligand displayed topoisomerase I activity inhibition and self-fluorescenc
17 the active site region of the mutant E. coli topoisomerase I activity shifted the pH for optimal acti
21 somes with camptothecin (CPT)-stabilized DNA-Topoisomerase I adducts activates an ATR-dependent pathw
23 ing this assay, we found that all the tested topoisomerase I and II (TOP1 and TOP2, respectively) poi
25 mage, and DNA-protein cross-links (including topoisomerase I and II cleavable complexes) produce stal
26 ations together, our study demonstrates that topoisomerase I and II may catalyze distinct steps of HB
27 nduction of DNA cross-linking, inhibition of topoisomerase I and II, and cell-cycle arrest at the S-p
28 e of the protein-protein interaction between topoisomerase I and RNA polymerase during stress respons
30 a distinct mechanism of interaction between topoisomerase I and RNA polymerase in Mycobacterium tube
32 consistent with negative feedback control of topoisomerase I and topoisomerase IV expression, which i
33 e evaluated for DNA binding propensities and topoisomerases I and II inhibition as part of their mech
36 ve for anti-RNA polymerase I/III, 5 for anti-topoisomerase I, and 8 for anticentromere, and 4 were no
37 NA re-ligation, diminishes the expression of topoisomerase I, and enhances the expression of inter al
38 rican patients were more likely to have anti-topoisomerase I (anti-topo I), anti-U1 RNP, and anti-U3
39 era containing autoantibodies against either topoisomerase I (anti-topo I; n = 12), nucleolar protein
40 PB1 alleles using DNA obtained from 318 anti-topoisomerase I antibody-positive patients and 561 healt
43 nd Senataxin (SETX), or by the inhibition of topoisomerase I, are actively processed into DNA double-
44 from the 5' side of a nick generated by DNA topoisomerase I at a ribonucleoside monophosphate residu
47 the widely expressed nuclear protein TOPORS (topoisomerase I-binding arginine/serine rich) are associ
49 uding ubiquitin-conjugating enzyme 9 (Ubc9); topoisomerase I-binding, arginine/serine-rich, E3 ubiqui
51 biomarkers such as carbonic anhydrase IX and topoisomerase I by immunohistochemistry show clear evide
53 DNA ends, like camptothecin-induced trapped-topoisomerase I, can be mediated by TDP1, BRCA1, CtIP an
54 we report the structure of Escherichia coli topoisomerase I catalytic domain (residues 2-695) in cov
55 Sera were tested for autoantibodies against topoisomerase I, centromere, and RNA polymerase I/III by
57 ncluding CTP, UTP, and GTP, had no effect on topoisomerase I cleavage and religation activities in th
59 single-stranded break associated with mutant topoisomerase I cleavage complex is converted to double-
60 cting Fe-S cluster formation protect against topoisomerase I cleavage complex-mediated cell killing.
62 ibited thymidylate synthase (TS) and trapped topoisomerase I cleavage complexes (Top1CCs), leading to
63 associated with a corresponding increase of topoisomerase I cleavage complexes and were further incr
65 d and decreased levels, respectively, of ARF/topoisomerase I complex and DNA-bound topoisomerase I.
66 predicted structural similarity to the human topoisomerase I core subdomains I and II (30-IXAla, 30-6
67 repair of substrates mimicking a 3'-blocked topoisomerase I covalent intermediate or an oxidative st
68 solved crystal structure of Escherichia coli topoisomerase I covalently linked to a single-stranded o
69 ogenic and/or lethal DNA damage in which the topoisomerase is covalently linked to the 3'- or 5'-term
70 , the release of torsional strain by type II topoisomerases is critical for converging replisomes to
72 also results from the action of calf-thymus topoisomerase I (CT Topo I) on a native supercoiled DNA
75 His(nuc)Ala (H182A) mutant actually induced topoisomerase I-dependent cytotoxicity and further enhan
77 rase I purified from camptothecin-stabilized topoisomerase I-DNA cleavage complexes in human breast c
81 soquinoline 5 and topotecan (2) bound in the topoisomerase I-DNA covalent complex, as well as molecul
83 othecins kill mammalian cells by stabilizing topoisomerase I-DNA strand passing intermediates that ar
86 NA binding domains to form diverse bacterial topoisomerase I enzymes that are highly efficient in the
87 features observed for MtTOP1 may allow these topoisomerase I enzymes to carry out physiological funct
89 significantly increased frequencies of anti-topoisomerase I, fibrillarin, and RNP autoantibodies com
90 in M. smegmatis competed with the endogenous topoisomerase I for protein-protein interactions with RN
92 The encounter of DNA replication forks with topoisomerase I-generated single-stranded DNA breaks res
93 ction, regions of the DNA polymerase and DNA topoisomerase I genes were amplified by PCR, sequenced a
94 ymerase I/III group, +13.4 years in the anti-topoisomerase I group, +11.1 years in the anticentromere
96 cal probe, we find that Escherichia coli DNA topoisomerase I has low RNA topoisomerase activity and t
97 OS-inducing mutants of Y. pestis and E. coli topoisomerase I have also been utilized as models to stu
98 l linkers, selective inhibitors of bacterial topoisomerase I, have been evaluated using bacterial cyt
99 topoisomerase II is both structurally (e.g., topoisomerase I, Hsp90, and kinases) and functionally (e
102 nitially hypersensitive to the inhibition of topoisomerase I/II and PARP, but acquire drug resistance
103 tance of liberating DNA termini from trapped topoisomerase is illustrated by the progressive neurodeg
107 p3beta differs from that of Escherichia coli topoisomerase I in that the former but not the latter re
108 rDNA and clarifies a structural role of DNA topoisomerase I in the epigenetic regulation of rDNA, in
109 n the essentiality of the topA gene encoding topoisomerase I in the model bacterium Bacillus subtilis
110 ported to promote the religation activity of topoisomerase I in the presence of camptothecin by itsel
111 Deficiency or depletion of mitochondrial topoisomerase I increased mitochondrial transcripts, whe
112 in inducing gammaH2AX response and repairing topoisomerase I-induced DNA damage as an alternative pat
113 hen gyrase, the sole T. thermophilus type II topoisomerase, is inhibited, TtAgo allows the bacterium
114 ction by either transcription termination or topoisomerase I inhibition has been shown to increase pa
116 ochondrial inhibitors, intracellular ROS, or topoisomerase I inhibition orchestrates an inflammatory
117 yl side chains display excellent E. coli DNA topoisomerase I inhibition properties with IC50 values <
118 n synthesized and their Escherichia coli DNA topoisomerase I inhibition, binding to B-DNA duplex, and
119 nt anticancer activity do not exhibit strong topoisomerase I inhibition, suggesting a separate mechan
120 RC stress response was also activated by the topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin
121 circadian toxicity patterns of irinotecan, a topoisomerase I inhibitor active against colorectal canc
124 nd PRC2 exhibit synthetic sensitivity to the topoisomerase I inhibitor Camptothecin and accumulate ga
125 h clinically-relevant nanomolar doses of the Topoisomerase I inhibitor camptothecin, loss of WRN exon
126 ries, Abbott Park, IL), and the DNA-damaging topoisomerase I inhibitor camptothecin-11 (CPT-11) or SN
132 ) mice are hypersensitive to camptothecin, a topoisomerase I inhibitor that causes DNA damage primari
133 anticancer agent camptothecin (CPT) is a DNA topoisomerase I inhibitor that causes fork collapse and
135 reported that combining (131)I-MIBG with the topoisomerase I inhibitor topotecan induced long-term DN
137 n the present studies, an indenoisoquinoline topoisomerase I inhibitor was conjugated to DUPA via a p
138 latform, the effect of an apoptotic inducer, topoisomerase I inhibitor, 7-ethyl-10-hydrocamptothecin
140 ncer drug, and it is a prodrug of the potent topoisomerase I inhibitor, SN-38 (7-ethyl-10-hydroxycamp
141 s synthesized by conjugating camptothecin, a topoisomerase I inhibitor, to our proprietary, 'clickabl
142 raction of a PARP inhibitor, ABT-888, with a topoisomerase I inhibitor, topotecan, in PBMCs, tumor, a
146 an pegol (NKTR-102) is a unique, long-acting topoisomerase-I inhibitor with prolonged systemic exposu
147 rtical neurons from mice, we identify twelve topoisomerase I inhibitors and four topoisomerase II inh
150 p synthesis of a series of clinically active topoisomerase I inhibitors such as NSC 314622, LMP-400,
153 amage induced by chemotherapy drugs, such as topoisomerase I inhibitors, results in S and G2 phase ar
158 es with dual tyrosyl-DNA phosphodiesterase I-topoisomerase I inhibitory activity in one low molecular
159 und 14a was synthesized and found to possess topoisomerase I inhibitory activity that was slightly be
160 analogues for their MYC-inhibitory activity, topoisomerase I-inhibitory activity, and anticancer acti
161 topoisomerase I to demonstrate that the ARF/topoisomerase I interaction is regulated by topoisomeras
162 whether Top1mt, the vertebrate mitochondrial topoisomerase, is involved in this process, we studied l
172 hibited PARP-1/NAD-facilitated religation of topoisomerase I-linked DNA (TLD) in the presence of camp
173 tudy suggests that dual targeting of MYC and topoisomerase I may serve as a novel strategy for antica
179 duce expression of the corresponding E. coli topoisomerase I mutant (EcTOP-D111N) encoded on a high-c
181 y itself through the direct interaction with topoisomerase I or by the formation of poly(ADP-ribosyl)
182 patients who had either circulating anti-DNA topoisomerase I (P=7.58x10(-17)/4.84x10(-16)) or anticen
183 of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et
189 to a protein that potentiates the effects of topoisomerase I poisons by binding to damaged DNA and pr
190 veliparib to enhance the cytotoxicity of the topoisomerase I poisons topotecan and camptothecin (CPT)
195 This could be due to the suppression of topoisomerase I poly(ADP-ribosyl)ation through the compe
196 endogenous ubiquitin-family modifications of topoisomerase I purified from camptothecin-stabilized to
200 ximal to the active site tyrosine of type IA topoisomerases is required for the relaxation of superco
201 member of the conserved Type IA subfamily of topoisomerases, is required for the cell proliferation i
202 rine in Yersinia pestis and Escherichia coli topoisomerase I results in bacterial cell killing due to
203 /topoisomerase I interaction is regulated by topoisomerase I serine phosphorylation, a modification t
204 ants of Yersinia pestis and Escherichia coli topoisomerase I showed that DNA religation can be inhibi
205 sis of purified Y. pestis and E. coli mutant topoisomerase I showed that the Met to Arg substitution
206 bit Mg(2+) dependent religation by bacterial topoisomerase I specifically could be developed into use
208 of HIF-1alpha protein by UVC did not require topoisomerase I, suggesting a similar yet distinct mode
209 inhibitor, in combination with topotecan, a topoisomerase I-targeted agent, was carried out to deter
210 agent that produces oxidative DNA damage, or topoisomerase I-targeted drugs (camptothecin and a nonca
211 in vivo evaluation of the combination of DNA topoisomerase I-targeted drugs and mTOR kinase inhibitor
215 mutations in ribonuclease H, senataxin, and topoisomerase I that resolve RNA-DNA hybrids lead to inc
216 rase III is a more efficient decatenase than topoisomerase I, the opposite is true for DNA relaxation
217 is important to characterize the ability of topoisomerase I to cleave positively supercoiled DNA.
218 er cell lines and purified recombinant human topoisomerase I to demonstrate that the ARF/topoisomeras
220 The method is based on genetic tagging of topoisomerase I to immobilize the enzyme on a solid surf
221 phodiesterase-1 protects cells from abortive topoisomerase I (Top1) activity by hydrolyzing the 3'-ph
222 These deletion events are dependent on DNA topoisomerase I (Top1) and are initiated by Top1 incisio
225 ch as DNA replication and transcription, DNA topoisomerase I (Top1) catalyzes the relaxation of DNA s
232 the repair of damaged DNA resulting from the topoisomerase I (Top1) inhibitor camptothecin and a vari
233 gically transported from the indolocarbazole topoisomerase I (Top1) inhibitor class to the indenoisoq
236 ives, topotecan and irinotecan, are specific topoisomerase I (Top1) inhibitors and potent anticancer
242 Hydroxylated analogues of the anticancer topoisomerase I (Top1) inhibitors indotecan (LMP400) and
243 The aromathecin or "rosettacin" class of topoisomerase I (top1) inhibitors is effectively a "comp
245 entify predictors of cancer cell response to topoisomerase I (Top1) inhibitors, a widely used class o
246 DNA interstrand cross-linking (ICL) agents, topoisomerase I (TOP1) inhibitors, and in Holliday junct
247 In search for a novel chemotype to develop topoisomerase I (Top1) inhibitors, the pyrazolo[1,5-a]qu
250 ntaining wild-type and mutant alleles of DNA topoisomerase I (TOP1) into the haploid yeast gene-disru
257 ow rapid recruitment, within minutes, of DNA topoisomerase I (TOP1) to a large cohort of AR-regulated
258 e-strand breaks (DSBs) in cells depleted for Topoisomerase I (Top1), an enzyme that relaxes DNA super
259 transcription-associated damage in yeast is Topoisomerase I (Top1), an enzyme that removes torsional
260 ngle CrA-PdG adduct can form crosslinks with topoisomerase I (Top1), both directly and indirectly.
262 ver, in a RNase H2 knock-out yeast strain, a topoisomerase I (Top1)-dependent mutator effect develops
266 ellular enzyme that repairs the irreversible topoisomerase I (Top1)-DNA complexes and confers chemoth
267 A phosphodiesterase I (TDP1) repairs stalled topoisomerase I (Top1)-DNA covalent complexes and has be
268 This type of linkage is found at stalled topoisomerase I (Top1)-DNA covalent complexes, and TDP1
274 n nuclei and mitochondria, and mitochondrial topoisomerase I (Top1mt) is the only DNA topoisomerase s
276 that mutations in the gene encoding for DNA topoisomerase I (topA) give rise to mutator phenotypes w
278 mary cellular target of YjhX was found to be topoisomerase I (TopA), inhibiting both DNA replication
279 the spatiotemporal recruitment of GFP-tagged topoisomerase I (TopI) to sites of localized DNA damage
281 to camptothecin (CPT), impaired CPT-induced topoisomerase I (Topo I) degradation and ubiquitination,
282 Using an NKX3.1 affinity column, we isolated topoisomerase I (Topo I) from a PC-3 prostate cancer cel
285 e results of a phase I clinical trial of the topoisomerase I (Topo I) poison CPT-11 followed by the c
286 sor, p14ARF (ARF) is a positive regulator of topoisomerase I (topo I), a central enzyme in DNA metabo
288 nteraction between the C-terminal domains of topoisomerase I (TopoI-CTDs) and the beta' subunit of RN
289 Presently it is shown that in addition to topoisomerase I, topopyrones A-D also act as poisons of
292 discrimination by prokaryotic and eukaryotic topoisomerases is vital to therapeutic utility, but is p
294 herichia coli expressing SOS-inducing mutant topoisomerase I was utilized to demonstrate that covalen
297 oligonucleotides to Mycobacterium smegmatis topoisomerase I with progressive C-terminal deletions sh
299 In depth biochemical analysis of E. coli topoisomerase I with the corresponding Arg-321 mutation
300 opy-number plasmid clones of Yersinia pestis topoisomerase I (YpTOP) with Asp-to-Asn substitution at
301 with arginine in recombinant Yersinia pestis topoisomerase I (YTOP) was the only substitution at this