Disease relevance of GDP-bS

• Preincubation with pertussis toxin or guanyl-5'-yl thiophosphate inhibited the PDGF but not the EGF effect [1].

High impact information on GDP-bS

• However, using guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) to prevent the dissociation of the fMet-Leu-Phe-associated G-protein within electrically permeabilized cells, led to a pronounced reduction (62%) of the binding between ligand-receptor complexes and the cytoskeleton [2].
• AngII-mediated inhibition of bTREK-1 through the novel Ca2+-dependent pathway was blocked by the AT1 receptor antagonist losartan, or by including guanosine-5'-O-(2-thiodiphosphate) in the pipette solution [3].
• Pre-loading of cells with guanyl-5'-yl thiophosphate failed to prevent Abeta(1-42)-induced inhibition, suggesting that down-regulation of halpha4beta2-nAChR function by Abeta(1-42) is not mediated by nAChR internalization [4].
• Non-hydrolyzable ATP could substitute for ATP, and guanyl-5'-yl thiophosphate blocked the activation of the channel by IGF-I [5].
• The insulin effect on MAP kinase and PP-1 activation was blocked by a GTP antagonist, guanyl-5'-yl thiophosphate [6].

Chemical compound and disease context of GDP-bS

• The intracellular perfusion of a broad G-protein inactivator, guanosine-5'-O-(2-thiodiphosphate) (GDP beta S), abolished adenosine-evoked currents, whereas a Gi/Go-protein inhibitor, pertussis toxin, had no effect [7].
• 4. Pertussis toxin mediated [32P]ADP-ribosylation was enhanced by ATP, ADP, adenylyl imidodiphosphate, GTP, guanosine-5'-O-(2-thiodiphosphate), guanosine-5'-O-(3-thiotriphosphate), and NaF but not AMP or guanylyl imidodiphosphate [GMP-P(NH)P] [8].

Biological context of GDP-bS

• The GDP analogue guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) caused a 70% inhibition of the bombesin-induced phosphorylation of Mr 80,000 protein but had no effect on the phosphorylation induced by PDBu [9].
• Both the loss of muscarinic acetylcholine receptors and activation of phosphoinositide hydrolysis in permeabilized cells were inhibited by the inclusion of guanosine-5'-O-(2-thiodiphosphate) [10].

Anatomical context of GDP-bS

• Guanosine-5'-O-(2-thiodiphosphate) (GDP-beta-S; a metabolically stable analog of guanosine diphosphate [GDP] that inactivates the G protein) and the carrier medium (CM; medium in which the injected compounds were dissolved) were significantly less effective in oocyte activation [11].
• Treatment of macrophages with guanyl-5'-yl thiophosphate prior to GTP-gamma-S treatment abolished the GTP-gamma-S-potentiated increase in IP(3) levels in 8G1-treated macrophages [12].

Associations of GDP-bS with other chemical compounds

• Guanosine 5'-(3-O-thio)triphosphate enhanced while guanyl-5'-yl thiophosphate attenuated the DA-1 agonist-stimulated PL-C activity [13].
• The effect of Ang II on ERK1/2 phosphorylation was blocked by Ang II type 1 receptor antagonists, RNH6270 and PD98059 but not by SB203580 or Guanosine-5'-O-(2-ThioDiphosphate), a G-protein inhibitor [14].

Gene context of GDP-bS

• GTP and guanylyl-5'-imidodiphosphate stimulated yeast adenylate cyclase, while a GDP analog, guanosine-5'-O-(2-thiodiphosphate), competitively inhibited this stimulation [15].
• We have studied the effect of GDP and its analog guanyl-5'-yl thiophosphate (GDP beta S) on the interaction between rhodopsin and transducin (Gt) [16].
• Stimulation of phospholipase C activity was abolished by guanosine-5'-O-(2-thiodiphosphate), confirming the involvement of a G protein-coupled receptor [17].
• Guanosine-5'-O-(2-thiodiphosphate) inhibited the response to forskolin (-38%) and to low doses of glucagon (-50%) [18].
• Furthermore, guanosine-5'-O-(2-thiodiphosphate) blocked the VIP receptor-mediated effect on the IKin [19].

Analytical, diagnostic and therapeutic context of GDP-bS

• Whole-cell recordings of IM were made from isolated bullfrog sympathetic neurons to examine the effects of intracellularly applied guanosine-5'-O-(2-thiodiphosphate) (GDP beta S) on agonist inhibition of IM [20].

References