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1 ) ACAP1 onto the endosome in the presence of aluminum fluoride.
2 nce of the ATP transition state analogue ADP-aluminum fluoride.
3 nted the increase in PKD activity induced by aluminum fluoride.
4 as the transitional state of Rop mimicked by aluminum fluoride.
5 e GAP domain with the GDP-bound Rop, as does aluminum fluoride.
6 vated by the beta-adrenergic receptor and by aluminum fluoride.
7 nzymatically activated in cells treated with aluminum fluoride.
8 o alpha-agarose and eluted specifically with aluminum fluoride.
9 ilament generated in the presence of ATP and aluminum fluoride.
10 ng was achieved by the formation of an (18)F-aluminum fluoride ((18)F-AlF) complex, and (64)Cu labeli
12 cate that the transition state analog, MgADP-aluminum fluoride-acetate, forms an abortive complex in
13 ing cell lysates revealed that RGS3 bound to aluminum fluoride-activated Galpha11 and to a lesser ext
14 50 values of 30 and 96 nM, respectively, for aluminum fluoride-activated wild type alphao and alphai1
15 hown to indirectly activate the ARF1 GTPase, aluminum fluoride (AIF) treatment of ARF6-transfected ce
16 describe 4 new probes using either (64)Cu or aluminum fluoride (Al(18)F) chelated to 2 NOTA derivativ
19 the alphaT*(R238E) mutant did not respond to aluminum fluoride (AlF4(-)), as read out by changes in T
20 sults in decreased activation by receptor or aluminum fluoride (AlF4-) and increased basal GDP releas
21 t with TGF alpha and the G protein activator aluminum fluoride (AlF4-), we determined if TGF alpha or
22 ch as vanadate, beryllium fluoride (BeFx) or aluminum fluoride (AlF4-), yields stable complexes which
25 ivators PspF and NifA in the presence of ADP-aluminum fluoride, an analog of ATP in the transition st
26 nding of phosphate, or the phosphate analogs aluminum fluoride and beryllium fluoride, to actin filam
27 ass II-containing complexes was inhibited by aluminum fluoride and brefeldin A, indicating the involv
28 nd (15)N-ChiT in the presence and absence of aluminum fluoride and guanosine 5'-3-O-(thio)triphosphat
29 of vanadate trapped MgADP (MgADPVi-S1) with aluminum fluoride and scandium fluoride trapped MgADP (M
31 constituted with G(betagamma) as assessed by aluminum fluoride-dependent changes in intrinsic tryptop
34 Ca(2+)-ATPases to form stable complexes with aluminum fluoride (E2.AlF) and beryllium fluoride (E2.Be
38 tide binding or hydrolysis, or activation by aluminum fluoride, indicating that the effects on recept
40 on of cofilin phosphorylation in response to aluminum fluoride induction in B16-F1 cells, which event
41 e phosphate analogues beryllium fluoride and aluminum fluoride led to complete inhibition of ATPase a
42 lipid vesicles was observed upon addition of aluminum fluoride or excess unlabeled alpha subunit, ind
43 n, but activation of F-alpha with either GDP/aluminum fluoride or guanosine 5'-O-(3-thiotriphosphate)
44 and gamma-phosphate analogues (beryllium and aluminum fluoride) or when dialyzed into guanosine 5'-3-
45 Activation of G proteins by treatment with aluminum fluoride produced an accumulation within the er
46 o first-order inhibition is dependent on the aluminum fluoride species, AlF4, and is linear with [Al]
47 rresponding reduction in charge in the bound aluminum fluoride species, which changes to a trifluoroa
51 ls injected with GTPgammaS or incubated with aluminum fluoride, suggesting a general role for GTPases
52 e) or 5'-adenylylimido-diphosphate), ADP, or aluminum fluoride that is postulated to trap ATPases at
55 rescence and subcellular fractionation after aluminum fluoride treatment, suggesting that it occurs w
57 P-1 remained cytosolic in cells treated with aluminum fluoride unless the cells were preincubated wit
58 Region I to activator in the presence of ADP-aluminum fluoride was shown and inferred from in vivo su
59 lpha(T)(*) linker mutants were responsive to aluminum fluoride, which binds to alpha-GDP complexes an
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