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1 o identify PIWIL3 as a mechanistic target of enoxacin.
2 sponses to standard-of-care chemotherapy and enoxacin.
3 corrected by exposure to the fluoroquinolone enoxacin.
4 tin was altered in cells treated with 50 muM enoxacin.
5 roquinolones norfloxacin, ciprofloxacin, and enoxacin.
6  in the presence of gyrase and the quinolone enoxacin.
7                                              Enoxacin (50 muM) did not induce apoptosis as measured b
8 orption is red-shifted (lambdamax 670 nm for enoxacin, 700 nm for ciprofloxacin and norfloxacin).
9                           Cells treated with enoxacin, a compound previously demonstrated to augment
10                                              Enoxacin, a fluoroquinolone antibiotic, was identified a
11                         We hypothesized that enoxacin acts directly and specifically on osteoclasts b
12 ily subcutaneous injections of enoxacin, bis-enoxacin, alendronate, or doxycycline were administered
13 ctam (ampicillin and penicillin), quinolone (enoxacin), aminoglycoside (kanamycin and neomycin), and
14 ingly, the bone-targeted antiresorptives bis-enoxacin and alendronate inhibited increases in oxidativ
15 d characterizing stable ternary complexes of enoxacin and CcdB protein with gyrase bound to a strong
16                                              Enoxacin and entinostat were the most effective adjuvant
17                    Three differences between enoxacin- and CcdB-derived complexes were discovered.
18  2) Complexes that produce DNA cleavage with enoxacin are reversible, whereas similar complexes made
19 erent diseases, and the feasibility of using enoxacin as a chemical template for inspiring medicinal
20 ional agent not yet FDA-approved, we propose enoxacin as an adjuvant drug for further preclinical and
21           Herein, the biological activity of enoxacin as SMER is discussed to shed light on its innov
22 a bisphosphonate derivative of enoxacin, bis-enoxacin (BE), which was previously studied as a bone-di
23                              However, unlike enoxacin, BE stimulated caspase-3 activity.
24                                           1) Enoxacin binds to the DNA active site and alters the bre
25 thesized that a bisphosphonate derivative of enoxacin, bis-enoxacin (BE), which was previously studie
26             Daily subcutaneous injections of enoxacin, bis-enoxacin, alendronate, or doxycycline were
27 ified and in vitro testing demonstrated that enoxacin blocked binding between purified B2 and microfi
28  substrates (norfloxacin, ciprofloxacin, and enoxacin) by varying the pH between 6 and 9 while the ch
29 he pulse (lambdamax 520, 610, and 620 nm for enoxacin, ciprofloxacin, and norfloxacin, respectively).
30                           Our data show that enoxacin directly inhibits osteoclast formation without
31                                              Enoxacin dose dependently reduced the number of osteocla
32             Consistent with this hypothesis, enoxacin dose-dependently reduced the number of multinuc
33 tumor cells were subjected to treatment with enoxacin, doxorubicin, or both drugs.
34                                              Enoxacin has been identified as a small molecule inhibit
35 ecting aberrant T-cell miRNA expression with enoxacin in dnTGFBRII mice could modulate autoreactive T
36 , danofloxacin, ofloxacin, sarafloxacin, and enoxacin) in environmental water samples, by fusing two
37                                              Enoxacin increases miRNA expression in dnTGFBRII CD8 T c
38  Notably, augmented DNA repair stimulated by enoxacin increases the survival also of cancer cells tre
39 hanisms can be explained by a model in which enoxacin induces formation of a novel "cleavable" comple
40                                              Enoxacin inhibited osteoclast formation at concentration
41                                              Enoxacin inhibits binding between the B-subunit of vacuo
42                                  In summary, enoxacin is a novel small molecule inhibitor of osteocla
43                                              Enoxacin is a small molecule fluoroquinolone that enhanc
44                                              Enoxacin is a small molecule that stimulates RNA interfe
45                          In the context that enoxacin is an FDA-approved antibiotic, and that entinos
46 nhancing DICER activity by a small molecule, enoxacin, is beneficial for neuromuscular function in tw
47   BE shared a number of characteristics with enoxacin: It blocked binding between the recombinant B-s
48                                              Enoxacin, kanamycin, neomycin, and tetracycline show syn
49 NAi pathway and find that the small-molecule enoxacin (Penetrex) enhances siRNA-mediated mRNA degrada
50                               Treatment with enoxacin reduced the association of V-ATPase subunits wi
51                                              Enoxacin significantly decreased CD8 T-cell expression o
52                                           3) Enoxacin stimulates cleavage of both relaxed and superco
53                                              Enoxacin stimulates DDRNA production at chromosomal DSBs
54           Here, we used alkenox, a clickable enoxacin surrogate, coupled with quantitative mass spect
55                                              Enoxacin treatment directly altered T cells both ex vivo
56                 Flow cytometry revealed that enoxacin treatment favored the expression of high levels
57                                              Enoxacin treatment significantly up-regulated miRNAs in
58               Quantitative PCR revealed that enoxacin triggered significant reductions in several ost
59 ed 53BP1 occupancy at DNA lesions induced by enoxacin ultimately suppresses homologous recombination,
60                                      BE, bis-enoxacin; V-ATPase, vacuolar H(+)-ATPase; TRAP, tartrate
61                                              Enoxacin was reported as the first and unique small-mole
62                                  Conversely, enoxacin, which enhances miRNA maturation by stimulating
63                                          Bis-enoxacin, which has both antiresorptive and antibiotic a