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1 myc followed by treatment of cells with N-(6-aminohexyl)-1-naphthalenesulfonamide, a calmodulin inhib
3 -yl)amino)hexyl]-2,5-pyrro lidinedione; N-(6-aminohexyl)-1-naphthalenesulfonamide; N-(4-aminobutyl)-1
4 ), but not their less-active analogues (N-(6-aminohexyl)-1-naphthalenesulfonamide; promethazine), wer
5 stitutions of the zwitterionic residues 5-(6-aminohexyl)-2'-deoxycytidine, 5-(6-aminohexyl)-2'-deoxyu
6 dues 5-(6-aminohexyl)-2'-deoxycytidine, 5-(6-aminohexyl)-2'-deoxyuridine, or 5-(3-aminopropyl)-2'-deo
7 ivation in striated muscle, we employed n-(6-aminohexyl) 5-chloro-1-napthalenesulfonamide (W7) as an
9 protein gene transcripts decreased with N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide and stauro
10 rogenase, moniliformin, of calmodulins, N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide, and of ca
11 tetraacetoxymethyl ester (BAPTA/AM) or N-(6-aminohexyl)-5-chloro-1-naphtalenesulfonamide (W7) before
12 -P cells with the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphtha-lenesulfonamide hydrochlo
13 e data show that three CaM antagonists (N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide, tamoxife
14 lucose transport response to hypoxia or N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) (whi
16 ompromised by the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) but
17 ctivity and the calcium releasing agent N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W7; 100 m
18 inhibitory effect of the CaM antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochlor
19 modulin antagonists trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide inhibited
20 -10 cells with a calmodulin antagonist (N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, HCl) resu
21 nts, including the calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, phenothia
23 )-octyl-3,4,5-trimethoxybenzoate), CaM (N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide; N-(4-amin
25 microM of the calmodulin antagonist W7 (N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide hydrochlo
27 of these substances demonstrates that the 4'-aminohexyl-5,7-dyhydroxyflavone 10 is a potent competiti
28 But, exposing them to 0.1 micromol/l n-[6-aminohexyl]-5-chloro-1-naphthalene-sulfonamide, a calmod
29 r calmodulin-dependent protein kinases (N-[6-aminohexyl]-5-chloro-1-napthalenesulfonamide, Lavendusti
30 nce spectroscopy using the PARG inhibitor 8-(aminohexyl)amino-ADP-HPD demonstrated that the binding c
31 ',5'-cyclic monophosphate) or domain B (8-(6-aminohexyl)aminoadenosine-3',5'-cyclic monophosphate) in
32 accharide intermediate to give the hexyl and aminohexyl analogues also led to unexpected results.
33 , to be used as a soluble inhibitor, and the aminohexyl glycoside analogue, to be conjugated to prote
34 a soluble inhibitor hexyl glycoside, as a 6-aminohexyl glycoside for conjugation to proteins, and as
35 e inhibitors in binding studies and two as 6-aminohexyl glycosides to be conjugated to carrier protei
36 lex stability by 1.6- or 13-fold, whereas an aminohexyl group or intercalating agent (acridine or pso
37 Inhibitor 3, which does not incorporate an aminohexyl group that can interact with the S1 subsite,
41 her N-[7-nitrobenz-2-oxa-1, 3-diazol-4-yl]-6-aminohexyl ouabain or 5-(and-6)-carboxyfluorescein-6-ami
42 and N-[7-nitrobenz-2-oxa-1, 3-diazol-4-yl]-6-aminohexyl ouabain was 29.2% in the microsomes compared
43 canoyl chain produced the dipeptide p-(omega-aminohexyl)phenacetyl-L-seryl-L-lysyl-N-(cyclohexyleth y
44 b provided the dipeptide analog [2-[p-(omega-aminohexyl)phenyl]propionyl]-L-seryl-L-lysyl-N-(cyclohex
45 e) conjugate, biotin-HDAAMP (adenosine 5'-(6-aminohexyl) phosphoramide; where HDA is 1,6-hexanediamin
46 ose column chromatography, F420-ether-linked aminohexyl-Sepharose 4B affinity chromatography, and qua
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