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1 hypusine synthase competitive inhibitor N(1)-guanyl-1,7-diaminoheptane (GC(7))is observed bound withi
2 injections of the deoxyhypusine inhibitor N1-guanyl-1,7-diaminoheptane (GC7) demonstrated significant
3        Pharmacologic targeting of DHPS by N1-guanyl-1,7-diaminoheptane (GC7) or RNA interference-medi
4      In vitro, inhibition of DHPS using N(1)-guanyl-1,7-diaminoheptane or shRNA resulted in a decreas
5                                     S-[2-(N7-guanyl)[2H4]-ethyl] glutathione was synthesized and used
6 of signal transduction through G proteins by guanyl-5'-beta-thiophosphate revealed that the effect of
7 timulated by isoproterenol, sodium fluoride, guanyl-5'-imidodiphosphate, and forskolin in hypoxic mem
8 esensitization in response to isoproterenol, guanyl-5'-imidodiphosphate, or forskolin.
9 d NIH 3T3 cells was found to be activated by guanyl-5'-yl imidodiphosphate (GMPPNP) and was identifie
10 y complex [14C]Phe-tRNA-elongation factor Tu.guanyl-5'-yl imidodiphosphate) but not [14C]Phe-tRNA.elo
11 cked by G-protein inhibition by injection of guanyl-5'-yl thiophosphate and by pre-stimulation of pho
12                    Pre-loading of cells with guanyl-5'-yl thiophosphate failed to prevent Abeta(1-42)
13          We show that pre-loading cells with guanyl-5'-yl thiophosphate fails to prevent this inhibit
14 h injection of oocytes with either GDPbetaS (guanyl-5'-yl thiophosphate) or GTPgammaS (guanosine 5'-3
15 (gamma-thiotriphosphate), and histamine plus guanyl-5'-yl thiophosphate, implying that histamine incr
16 uced by the cationic trans-8,9-dihydro-8-(N7-guanyl)-9-hydroxy-aflatoxin B(1) adduct.
17  DNA adduct of AFB(1) is 8,9-dihydro-8-(N(7)-guanyl)-9-hydroxyaflatoxin B(1) (AFB(1)-N7-Gua), which i
18 eotide containing a single 8,9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N7-Gua) adduct was i
19 ally and thermally labile 8,9-dihydro-8- (N7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N7-Gua) adduct, the
20 he initially formed trans-8, 9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1 adduct under basic conditi
21 appa was studied with a series of eight N(2)-guanyl adducts (in oligonucleotides) ranging in size fro
22 e results are consistent with a role of N(7)-guanyl adducts in mutagenesis.
23 toactivated azide formed primarily C8 and N2 guanyl adducts.
24  for the left/right asymmetric expression of guanyl cyclase (gcy) genes in two chemosensory neurons t
25 aacetic acid acetoxymethyl ester, and by the guanyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quin
26 luding hypoxia-inducible factor and atypical guanyl cyclase sensing of oxygen, with downstream action
27 ptide and blocked by a specific inhibitor of guanyl cyclase, 1H-(1,2,4)oxadiazolo[4,3, -a]quinoxalin-
28 inhibitors of nitric oxide synthase, soluble guanyl cyclase, or PKG after nerve injury, and found tha
29 with NP clearance receptors, but not with NP guanyl cyclase-coupled signaling receptors, we demonstra
30 ection and quantitative analysis of S-[2-(N7-guanyl)ethyl]glutathione as a DNA adduct formed upon exp
31                                 RasGRP2 is a guanyl exchange factor for Rap1.
32 complexes, GKy x Mg(II)ADP x [U-13C]GMP, the guanyl glycosidic torsion angle, chi, is 50 +/- 5 degree
33 trate complexes, GKy.MgADP.[u-(13)C]GMP, the guanyl glycosidic torsion angle, chi, is 51 +/- 5 degree
34 uoroornitithine) and MGBG [methylgloxal-bis (guanyl hydrazone)].
35 ral diminazene-inspired diaryl mono- and bis-guanyl hydrazones.
36 es in nonhuman primates with [11C]1e, N-[11C]guanyl-m-octopamine, which has a slow NET transport rate
37                                      N-(11)C-guanyl-(-)-meta-octopamine ((11)C-GMO) has a much slower
38 urrence of the second messenger 3',5'-cyclic guanyl monophosphate (cGMP) has been shown in a number o
39 d to increase concentrations of 3',5'-cyclic guanyl monophosphate in both pollen and leaves, as detec
40 ut the amide (gamma) (14.4 kcal/mol) and the guanyl-nitrogen (alpha) bonds.
41 -loop corresponding to Ras(Ser-17) abolishes guanyl nucleotide binding.
42 x in vivo and in vitro does not require Rheb guanyl nucleotide charging but is modulated by GTP and i
43 ORC1 in vitro is entirely independent of Rag guanyl nucleotide charging.
44 1 activation is due to the regulation of Rag guanyl nucleotide charging.
45 apoprotein activity was investigated using a guanyl nucleotide exchange assay on transducin.
46                In this system, the mammalian guanyl nucleotide exchange factor (GEF) Sos is recruited
47  the small adaptor protein Grb2 with the Ras guanyl nucleotide exchange factor SOS is functionally im
48 uitment of GAPEX-5, a VPS9 domain-containing guanyl nucleotide exchange factor that forms a complex w
49 he GTP binding of RalA by recruiting the Ral guanyl nucleotide exchange factor, Rlf/Rgl2.
50 protein RasGRP belongs to the CDC25 class of guanyl nucleotide exchange factors that regulate Ras-rel
51 1 or Mst2, Mob1 binds and activates the Rac1 guanyl nucleotide exchanger Dock8, which is abundant in
52 mTOR to Rheb mutants that are unable to bind guanyl nucleotide in vivo is also inhibited by amino wit
53  surprising in view of the minimal impact of guanyl nucleotide on Rheb switch 2 configuration.
54 rget cells (HA1 fibroblasts) occurred in all guanyl nucleotide-containing pools examined following ex
55                                          The guanyl nucleotide-releasing protein (GRP) family members
56                                          Ras guanyl nucleotide-releasing protein (GRP) was recently i
57 tudy, we find that B1 cells express only Ras guanyl nucleotide-releasing protein (RasGRP) 1, whereas
58        We identified a new member of the Ras guanyl nucleotide-releasing protein (RasGRP) family of R
59 expressed SOS and specifically expressed Ras guanyl nucleotide-releasing protein (RasGRP).
60        Previous studies demonstrate that Ras guanyl nucleotide-releasing protein (RasGRP)1 is essenti
61 uating the function of the DAG-dependent Ras guanyl nucleotide-releasing proteins (RasGRPs).
62 ) is regulated in part by the heterotrimeric guanyl-nucleotide binding protein (G protein) Goalpha.
63 e/threonine protein kinase) and Rom2 (a Rho1 guanyl-nucleotide exchange factor) from Cryptococcus neo
64  Ca2+-stimulated Ras activator Ras-GRF1 (Ras-guanyl-nucleotide releasing factor), and ERK.
65  cellular responses is SopE, which acts as a guanyl-nucleotide-exchange factor on Rho GTPase proteins
66 xhibit a very rapid, spontaneous exchange of guanyl nucleotides and an inability to hydrolyze GTP.
67 or adenyl nucleotides over the corresponding guanyl ones was observed.
68 siological pH values, the reduction of a DNA guanyl radical involves the transfer of a proton as well
69                                              Guanyl radical species are produced in DNA by electron r
70      Rate constants for the reduction of DNA guanyl radicals by these indoles can be calculated from
71 ular rate constants for the reduction of DNA guanyl radicals by these phenols.
72                                          DNA guanyl radicals can be reduced by electron donation from
73                             We have produced guanyl radicals in DNA by using the single electron oxid
74 larly tryptophan derivatives react to repair guanyl radicals in plasmid DNA with rate constants in th
75           We have examined the reactivity of guanyl radicals in plasmid DNA with the six most easily
76 sence of thiocyanate ions, we have generated guanyl radicals in plasmid DNA.
77 radiation of aqueous thiocyanate) to produce guanyl radicals in plasmid DNA.
78 ity of derivatives of these amino acids with guanyl radicals located in plasmid DNA.
79                                              Guanyl radicals, the product of the removal of a single
80 ctivation of LKB1 required expression of RAS guanyl releasing protein 3 (RASGRP3).
81                                      The Ras guanyl releasing protein RasGRP belongs to the CDC25 cla
82  through transcriptional upregulation of RAS guanyl-releasing protein 1 (RASGRP1) by PPARbeta/delta.
83     In this study we defined the role of Ras guanyl-releasing protein 1 (RasGRP1) in the development
84 ose alternate targets of DAG/PE effects, Ras guanyl-releasing protein 1 (RasGRP1), mediates the PE-in
85         We investigated whether RasGRP3 (Ras guanyl-releasing protein 3), a Ras activator expressed i
86 ied the culprit mutation (cG742T) in the RAS guanyl-releasing protein-2 (RASGRP2) gene coding for cal
87    Binase, a member of a family of microbial guanyl-specific ribonucleases, catalyzes the endonucleot
88 The structures of the (R)- and (S)-alpha-(N2-guanyl)styrene oxide adducts at X6 in d(GGCAGXTGGTG).d(C
89  search identified it as mannose-1-phosphate guanyl transferase (OsMPG1) gene from rice.