戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 terminant of improved insulin sensitivity by amlexanox.
2                                     However, amlexanox, a compound that is known to attenuate actin s
3 an anti-allergic and anti-inflammatory drug, amlexanox (AMX).
4                          Here we report that amlexanox, an approved small-molecule therapeutic presen
5 S100A13 binds the anti-inflammatory compound amlexanox and FGF-1 is involved in inflammation, we exam
6                                              Amlexanox binds S100A13 and inhibits the release of fibr
7 ast, the inhibition of cell proliferation by amlexanox correlates with the inhibition of cyclin D1 ex
8 ll migration and proliferation, and although amlexanox does not induce either the down-regulation of
9                 Treatment of obese mice with amlexanox elevates energy expenditure through increased
10 dy demonstrates the potential of repurposing amlexanox for the treatment of patients with RDEB harbor
11              These findings demonstrate that amlexanox improved metabolic health via FGF21 action in
12                                              Amlexanox increased COL7A1 transcript and the phosphoryl
13                                              Amlexanox increased FGF21 synthesis and secretion in sev
14 x to modify the cytoskeleton and report that amlexanox induces a dramatic reduction in the presence o
15                             Correspondingly, amlexanox induces the complete and reversible non-apopto
16 onsense-mediated mRNA decay, suggesting that amlexanox inhibits nonsense-mediated mRNA decay in cells
17 Because of its record of safety in patients, amlexanox may be an interesting candidate for clinical e
18 to partially rescue cells from the effect of amlexanox on both the actin cytoskeleton and cell migrat
19 in mediating the acute metabolic benefits of amlexanox on glucose metabolism, and point to a new ther
20  in inflammation, we examined the effects of amlexanox on the release of FGF-1 and p40 Syn-1 in respo
21  that treatment with the IKKe/TBK1 inhibitor amlexanox produces weight loss and relieves insulin resi
22           Accordingly, inhibition of TBK1 by amlexanox reduced p62 aggregates and restored NSC mainte
23 ses by treatment of obese mice with the drug amlexanox reversed obesity-induced catecholamine resista
24 ation with shRNA or small-molecule inhibitor amlexanox selectively inhibited the viability of NSCLC c
25 techolamine sensitivity in obese adipocytes, amlexanox stimulates adipocyte-specific IL-6 secretion.
26                         Last, the ability of amlexanox to inhibit FGF1 release is reversible and corr
27 the cytoskeleton, we examined the ability of amlexanox to modify the cytoskeleton and report that aml
28                                        While amlexanox treatment caused a transient reduction in food
29 cute inhibition of IKK-epsilon and TBK1 with amlexanox treatment increases cAMP levels in subcutaneou
30 in fasting blood glucose observed with acute amlexanox treatment were mediated by the suppression of
31                         We report that while amlexanox was able to repress the heat shock-induced rel
32                   Here the FDA-approved drug amlexanox was tested for its ability to read-through PTC
33      In vivo studies revealed that combining amlexanox with MEK inhibitor AZD6244 significantly inhib