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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
6  HDAC11's enzymatic activity is inhibited by trapoxin, a known histone deacetylase inhibitor.
7                                            A trapoxin affinity matrix was used to isolate two nuclear
8 istone deacetylase, the cyclic tetrapeptides trapoxin and Helminthsporium carbonum toxin (HC toxin),
9  promoter region is required for response to trapoxin and trichostatin.
10 ylase activity is inhibited by trichostatin, trapoxin, and butyrate in vitro to the same degree as th
11 trichostatin A, hydroxamic acid analogues of trapoxin, and scriptaid and its analogues.
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
14                                              Trapoxin B, a weak HDAC6 inhibitor, and calyculin A, a c
15               HDAC6, which is insensitive to trapoxin B, specifically interacted with the carboxy ter
16 cetylase inhibitor trichostatin A but not to trapoxin B.
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-
19                                              Trapoxin is a microbially derived cyclotetrapeptide that
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
26                                              Trapoxin treatment, which induces histone hyperacetylati
27 e occurs when 2-cell embryos are cultured in trapoxin, which is a specific and irreversible inhibitor

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