|1.||Schreiber, G: 2 articles (12/2001 - 07/2000)|
|2.||Avissar, S: 2 articles (12/2001 - 07/2000)|
|3.||Clack, James W: 1 article (07/2008)|
|4.||Yoo, Ki-Yeon: 1 article (01/2006)|
|5.||Won, Moo Ho: 1 article (01/2006)|
|6.||Shin, Hyung-Cheul: 1 article (01/2006)|
|7.||Hwang, In Koo: 1 article (01/2006)|
|8.||Kim, Do-Hoon: 1 article (01/2006)|
|9.||Jung, Boo Kyoung: 1 article (01/2006)|
|10.||Kang, Tae-Cheon: 1 article (01/2006)|
|1.||Alzheimer Disease (Alzheimer's Disease)
02/15/1995 - "MgCl2 enhanced [3H]OXO-M binding in both the occipital and temporal cortices of the Alzheimer's disease cases was reversed to control levels by Gpp[NH]p. "
02/09/1995 - "The guanine nucleotide analogue Gpp(NH)p inhibited binding by ca. 70% in both the control and Alzheimer's disease brains, the residual binding being sensitive to NaCl in both cases. "
11/25/1991 - "Gpp[NH]p reduced the [3H]8-OH-DPAT binding affinity and the number of binding sites to the same degree in both regions in control and Alzheimer's disease cases. "
11/01/1991 - "Analysis of the effect of Gpp[NH]p on [3H]clonidine saturation binding curves showed no significant differences between control and Alzheimer's disease samples in either frontal (Kd = 9.68 +/- 1.38, 9.1 +/- 2.6 nM; Bmax = 40.23 +/- 4.33, 44.3 +/- 9.4 fmol/mg, control and Alzheimer's disease values, respectively), or temporal (Kd = 11.61 +/- 4.04, 5.38 +/- 2.5 nM; Bmax = 52.0 +/- 14.0, 31.07 +/- 8.00 fmol/mg control and Alzheimer's disease values, respectively) cortices.(ABSTRACT TRUNCATED AT 250 WORDS)"
11/01/1991 - "The guanine nucleotide analogue, Gpp[NH]p inhibited [3H]clonidine binding in a concentration-dependent manner, the profiles of inhibition showing no significant differences between control and Alzheimer's disease samples. "
01/01/1984 - "Biodistribution and tumor uptake studies were carried out with intravenously injected tracer doses of Gpp(NH)p labeled with 3H, 32P or 99mTc . "
06/15/1988 - "Such as for the intact pituitary, the antagonist binding site density in 7315a tumors was not affected by NaCl and/or Gpp(NH)p, and its binding affinity was increased in the presence of NaCl. "
01/01/1984 - "Comparison of biodistribution of 3H, 32P and 99mTc labeled Gpp(NH)p in tumor bearing hamsters."
03/01/1988 - "The antagonist dopaminergic binding site in MtTW15 tumors labelled with [3H]spiperone remains unchanged at 25 degrees C in the presence or absence of sodium or guanine nucleotides (Gpp(NH)p); by contrast at 37 degrees C sodium increases the affinity while Gpp(NH)p decreases it slightly. "
08/31/1987 - "Guanosine 5'-[beta-gamma-imino]triphosphate (Gpp(NH)p) causes complete conversion of the high into low affinity dopaminergic agonist site in normal pituitary and in tumors. "
06/27/1995 - "GPP(NH)p inhibited binding of either [125I]Tyr4Bn or [125I]GRP at 24 h post infection, but not at 96 h post infection. "
12/01/1989 - "The increase in Vmax for ISPN determined in the presence of 5'-guanylylimidodiphosphate (Gpp[NH]p) was consistently lower in infected than in uninfected mice, suggesting that infection altered the potential synergistic activation of AC by the guanine nucleotide. "
04/01/1988 - "Another adenylate cyclase activity, which was stimulated by the nonhydrolyzable guanine nucleotide Gpp(NH)p, declines in relation to the duration of infection. "
04/01/1988 - "Inhibition of adenylate cyclase activity by adenosine and by Gpp(NH)p (in the presence of forskolin) declines after 21 days of infection. "
10/01/1987 - "Stimulating activities of adenylate cyclase due to isoproterenol, isoproterenol plus Gpp(NH)p, or forskolin (activities mediated by Ns) are not altered by infection. "
07/01/2003 - "Animals with heart failure exhibited depressions in ventricular function and AC activities in the absence or presence of forskolin, NaF and Gpp(NH)p. "
05/01/1991 - "Basal and Gpp(NH)p stimulated adenylate cyclase activity were decreased by 36% and 22% respectively in rabbits with heart failure as compared with control animals and cAMP production was significantly smaller in failing left ventricles than in control left ventricles both after NaF stimulation (C: 161.3 +/- 24.9 pmols/mg/min; HF: 98.8 +/- 7.0 pmols/mg/min; P less than 0.05) and even more after forskolin stimulation (C: 159.1 +/- 23.9 and HF: 60.8 +/- 7.3 pmols/mg/min; P less than 0.01). "
12/01/1985 - "Agonist displacement of [3H]dihydroalprenolol binding with isoproterenol in the presence and absence of 5'-guanylylimidodiphosphate [Gpp(NH)p] demonstrated a striking loss of high affinity binding sites in heart failure (51 +/- 16 to 11 +/- 5%). "
12/01/1985 - "Beta-Adrenergic receptor-mediated stimulation of adenylate cyclase and maximal stimulation with Gpp(NH)p or sodium fluoride was reduced in heart failure. "
08/11/1987 - "Congestive heart failure reduced the net production of cyclic AMP by isoproterenol, Gpp(NH)p, and forskolin in both the right and left ventricles, but did not alter the effect of manganese chloride. "
01/15/2006 - "Gpp(NH)p-dependent AC-I activity in hippocampal CA1 region was not changed in all groups, while Ca2+/calmodulin-dependent AC-I activity in hippocampal CA1 region was significantly decreased 24 h after ischemia-reperfusion. "
09/01/1994 - "Basal adenylyl cyclase activity was unchanged, but enzyme activity stimulated by the guanosine triphosphate analog guanyl-5'-imidodiphosphate (GppNHp) at 10 mumol/L was depressed 63% by ischemia (n = 16, p = 0.001). "
10/01/1998 - "In terms of AC activation, ischemia led to a marked increase (4-fold) in sensitivity to terbutaline (beta2-agonist) and phorbol ester (tetradecanoyl phorbol acetate = TPA) stimulation, whereas the dobutamine (beta1) responsiveness and Gpp(NH)p activation through G(s)alpha/G(i2)alpha remained unaltered. "
|1.||GTP-Binding Proteins (G-Protein)
|2.||Acetylcholine (Acetylcholine Chloride)
|3.||Muscarinic M2 Receptor
|6.||Adenylate Cyclase (Adenylyl Cyclase)
|9.||Guanosine Triphosphate (GTP)