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1 dulator tested in clinical trials is UCN-01 (7-hydroxystaurosporine).
2 n and enhanced with the checkpoint abrogator 7-hydroxystaurosporine.
3 n, ionizing radiation, hydrogen peroxide, or 7-hydroxystaurosporine.
5 tor, LY294002, and an Akt inhibitor, UCN-01 (7-hydroxystaurosporine), both synergistically sensitized
9 Akt pathway with the chemotherapeutic agent 7-hydroxystaurosporine prevented proliferation of vGPCR-
12 checkpoint abrogator and Chk1/Chk2 inhibitor 7-hydroxystaurosporine (UCN-01) also increases camptothe
13 1 (Chk1) in synergistic interactions between 7-hydroxystaurosporine (UCN-01) and mitogen-activated pr
14 nificantly attenuated by two PKC inhibitors, 7-hydroxystaurosporine (UCN-01) and N,N,N-trimethylsphin
15 nted by the protein kinase C (PKC) inhibitor 7-hydroxystaurosporine (UCN-01) but not by the Cdc2 inhi
16 e.g., PD184352) and the checkpoint abrogator 7-hydroxystaurosporine (UCN-01) dramatically induces apo
17 r agent and protein kinase C (PKC) inhibitor 7-hydroxystaurosporine (UCN-01) induces apoptosis indepe
19 endent kinase and protein kinase C inhibitor 7-hydroxystaurosporine (UCN-01) potentiates the cytotoxi
20 with regard to the efficacy of drugs such as 7-hydroxystaurosporine (UCN-01) that abrogate S and G(2)
21 e to the pharmacological agents caffeine and 7-hydroxystaurosporine (UCN-01) that inhibit the checkpo
22 The addition of the Chk1 kinase inhibitor 7-hydroxystaurosporine (UCN-01) to F-ara-A-arrested S-ph
23 bryostatin 1 and the PKC and Chk1 inhibitor 7-hydroxystaurosporine (UCN-01) were compared with respe
25 ely inhibited by checkpoint activation since 7-hydroxystaurosporine (UCN-01), the specific Chk1 inhib
26 ented by the cell-cycle checkpoint abrogator 7-hydroxystaurosporine (UCN-01), which markedly potentia
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