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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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