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1 ng HDAC inhibitors such as trichostatin A or trapoxin.
2 inding protein and site on that protein with trapoxin.
3 sitive to the specific deacetylase inhibitor trapoxin.
4 deacetylase inhibitors, trichostatin A, and trapoxin.
5 omes from the use of HDAC inhibitors such as trapoxin A (TPX), which leads to hyperacetylated histone
8 istone deacetylase, the cyclic tetrapeptides trapoxin and Helminthsporium carbonum toxin (HC toxin),
10 ylase activity is inhibited by trichostatin, trapoxin, and butyrate in vitro to the same degree as th
12 GCC) is critical for activation by butyrate, trapoxin, and trichostatin, whereas the proximal element
13 domains confers resistance to the inhibitors trapoxin B and sodium butyrate, which potently inhibit t
17 apoxin in vitro and the nuclear binding of a trapoxin-coumarin fluorophore in vivo, suggesting that d
18 It competitively inhibits the binding of [3H]trapoxin in vitro and the nuclear binding of a trapoxin-
20 cetylation associated with histone H3 in the trapoxin-responsive region of the p21(waf1) promoter.
21 specific inhibitors of histone deacetylase, trapoxin (TPX) and trichostatin A (TSA), to cause a glob
22 is inhibited in vitro by the small molecule trapoxin (TPX), and all three HDACs are retained by a TP
23 eacetylase, such as trichostatin A (TSA) and trapoxin (TPX), are potent inducers of HIV-1 transcripti
24 ells with the histone deacetylase inhibitor, trapoxin (TPX), resulted in selective changes in genes t
25 repression of a reporter gene is reduced by trapoxin treatment, suggesting that histone deacetylatio
27 e occurs when 2-cell embryos are cultured in trapoxin, which is a specific and irreversible inhibitor
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