ライフサイエンスコーパス: enoxacin

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1 sponses to standard-of-care chemotherapy and enoxacin.

2 corrected by exposure to the fluoroquinolone enoxacin.

3 o identify PIWIL3 as a mechanistic target of 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 Enoxacin, a fluoroquinolone antibiotic, was identified a

10 We hypothesized that enoxacin acts directly and specifically on osteoclasts b

11 ily subcutaneous injections of enoxacin, bis-enoxacin, alendronate, or doxycycline were administered

12 ctam (ampicillin and penicillin), quinolone (enoxacin), aminoglycoside (kanamycin and neomycin), and

13 ingly, the bone-targeted antiresorptives bis-enoxacin and alendronate inhibited increases in oxidativ

14 d characterizing stable ternary complexes of enoxacin and CcdB protein with gyrase bound to a strong

15 Three differences between enoxacin- and CcdB-derived complexes were discovered.

16 2) Complexes that produce DNA cleavage with enoxacin are reversible, whereas similar complexes made

17 a bisphosphonate derivative of enoxacin, bis-enoxacin (BE), which was previously studied as a bone-di

18 However, unlike enoxacin, BE stimulated caspase-3 activity.

19 1) Enoxacin binds to the DNA active site and alters the bre

20 thesized that a bisphosphonate derivative of enoxacin, bis-enoxacin (BE), which was previously studie

21 Daily subcutaneous injections of enoxacin, bis-enoxacin, alendronate, or doxycycline were

22 ified and in vitro testing demonstrated that enoxacin blocked binding between purified B2 and microfi

23 he pulse (lambdamax 520, 610, and 620 nm for enoxacin, ciprofloxacin, and norfloxacin, respectively).

24 Our data show that enoxacin directly inhibits osteoclast formation without

25 Enoxacin dose dependently reduced the number of osteocla

26 Consistent with this hypothesis, enoxacin dose-dependently reduced the number of multinuc

27 tumor cells were subjected to treatment with enoxacin, doxorubicin, or both drugs.

28 Enoxacin has been identified as a small molecule inhibit

29 hanisms can be explained by a model in which enoxacin induces formation of a novel "cleavable" comple

30 Enoxacin inhibited osteoclast formation at concentration

31 Enoxacin inhibits binding between the B-subunit of vacuo

32 In summary, enoxacin is a novel small molecule inhibitor of osteocla

33 Enoxacin is a small molecule that stimulates RNA interfe

34 nhancing DICER activity by a small molecule, enoxacin, is beneficial for neuromuscular function in tw

35 BE shared a number of characteristics with enoxacin: It blocked binding between the recombinant B-s

36 Enoxacin, kanamycin, neomycin, and tetracycline show syn

37 NAi pathway and find that the small-molecule enoxacin (Penetrex) enhances siRNA-mediated mRNA degrada

38 Treatment with enoxacin reduced the association of V-ATPase subunits wi

39 3) Enoxacin stimulates cleavage of both relaxed and superco

40 Here, we used alkenox, a clickable enoxacin surrogate, coupled with quantitative mass spect

41 Flow cytometry revealed that enoxacin treatment favored the expression of high levels

42 Quantitative PCR revealed that enoxacin triggered significant reductions in several ost

43 BE, bis-enoxacin; V-ATPase, vacuolar H(+)-ATPase; TRAP, tartrate

44 Conversely, enoxacin, which enhances miRNA maturation by stimulating

45 Bis-enoxacin, which has both antiresorptive and antibiotic a

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