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Chemical Compound Review

gamma-Thio-GTP     [(2R,3S,4R,5R)-5-(2-amino-6- oxo-3H-purin-9...

Synonyms: GTP-gamma-S, CHEBI:43000, GTP gamma S, AC1L1YFT, C01806, ...
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Disease relevance of gamma-Thio-GTP

  • Activation of a pertussis toxin-sensitive G protein by GTP-gamma-S blocked cGMP-kinase inhibition of the channel [1].
  • By contrast, the pretreatment with tetanus and botulinum B neurotoxins did not prevent GTP gamma S-stimulated insulin secretion [2].
  • Formation of runoff transcripts including retrovirus RNAs that normally contain 5'-m7GpppGmpC was not decreased by replacing GTP with non-hydrolyzable analogs, and Rous-associated virus-2 runoff products made in the presence of GTP-gamma-S contained 5'-terminal gamma-S-pppGpC [3].
  • We now report that G protein activation by GTP gamma S increases the Ba2+ conductance of high-voltage-activated Ca2+ channels of chick dorsal root ganglion (DRG) cells [4].
  • Incubation of isolated nuclei with Clostridium botulinum C3 exoenzyme inhibited the potentiating effect of GTP gamma S on ATP-dependent nuclear PLD activity [5].

Psychiatry related information on gamma-Thio-GTP

  • GTP gamma S-stimulated adenylyl cyclase activity was significantly lower in Alzheimer's disease superior temporal cortex, but not cerebellum, compared to values from a series of matched control cases [6].

High impact information on gamma-Thio-GTP

  • Interestingly, while the earliest steps in stack formation share some similarities with events catalyzing fusion of transport vesicles to its target membrane, neither GTP gamma S nor Rab-GDI, inhibitors of vesicular protein traffic, inhibit stack formation [7].
  • In cell lysates, GTP gamma S stimulated PIP 5-kinase activity, and this effect was blocked by botulinum C3 exoenzyme, suggesting that Rho was responsible [8].
  • A cytosolic factor markedly enhanced PLD activity in membranes and was essential for GTP gamma S-dependent stimulation of an enriched preparation of PLD [9].
  • We now report the complete purification of one component based on its ability to reconstitute GTP gamma S-mediated PLC activity and identify it as the phosphatidylinositol transfer protein (PI-TP) [10].
  • The BAPTA-inhibited step in fusion was biochemically distinct from, and occurred later than, the GTP gamma S-sensitive step mediated by the monomeric GTPase, ADP-ribosylation factor [11].

Chemical compound and disease context of gamma-Thio-GTP

  • The coupling is mediated by G proteins, since pertussis toxin treatment reduced the K+ current and injection of GTP gamma S (guanosine 5'-O-(thiotriphosphate)) enhanced it [12].
  • The activation of phospholipase C in human platelets is coupled to agonist receptors via guanine nucleotide-binding protein(s), and prior treatment of permeabilized platelets with GTP gamma S, GDP beta S, or pertussis toxin modifies platelet responses to agonists [13].
  • The absence of a significant rise in inositol 1-monophosphate indicated that phosphatidylinositol hydrolysis was not stimulated by AII or GTP gamma S. Pretreatment of glomerulosa cells with pertussis toxin for 12 h before permeabilization did not inhibit AII- or GTP gamma S-stimulated inositol polyphosphate formation [14].
  • Pertussis toxin completely inhibited the ZP-stimulated GTP gamma S binding, but only decreased mastoparan-stimulated GTP gamma S binding by 70-80% [15].
  • Overnight pretreatment with pertussis toxin or the addition of guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) or guanosine-5'-O-(2-thiodiphosphate) (GDP-beta-S) instead of GTP to the pipette solution did not alter this current, excluding involvement of G proteins [16].

Biological context of gamma-Thio-GTP


Anatomical context of gamma-Thio-GTP

  • Inhibition by GTP gamma S requires a cytosolic inhibitory factor that binds to Golgi membranes during inhibition [17].
  • Redistribution of both proteins can be prevented by pretreating cells with AlF4-. Recruitment of adaptors from the cytosol onto the TGN membrane has been reconstituted in a permeabilized cell system and is increased by addition of GTP gamma S and blocked by addition of BFA [22].
  • When this coating is exaggerated by GTP gamma S, the periphery of all cisternae is partitioned into coated vesicles that remain attached at their sites of formation [23].
  • Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers [19].
  • We report here that free GTP gamma S-activated G alpha i 1, but not G alpha i 2 or G alpha i 3, potently inhibits G beta 1 gamma 2-induced GIRK activity in excised membrane patches of Xenopus oocytes expressing GIRK1 [24].

Associations of gamma-Thio-GTP with other chemical compounds


Gene context of gamma-Thio-GTP

  • G(o) protein treated with GTP-gamma S lost the ability to associate with APP [30].
  • The addition of Sar1p promotes vesicle formation from the ER irrespective of the GTP- or GTP gamma S-bound form, indicating that the active form of Sar1p but not the hydrolysis of GTP is required for this process [31].
  • Actin incorporation in the bud can be stimulated by treating the permeabilized cells with GTP-gamma S, and, significantly, the stimulatory effect is eliminated by a mutation in CDC42, a gene that encodes a Rho-like GTP-binding protein required for bud formation [32].
  • The vesicles produced are functionally distinct from the ER: they transfer pro-alpha-factor to the Golgi apparatus faster and more efficiently than the ER, they do not require Sec12p or Sec23p to complete transfer, and transfer is resistant to GTP gamma S. Targeting of vesicles to the Golgi apparatus requires Ypt1p and Sec18p [33].
  • The weak stimulatory effect of ARF alone suggested that the GTP gamma S-stimulated PLD activity is dependent on the presence of another protein(s), presumably ARF-regulatory proteins [34].

Analytical, diagnostic and therapeutic context of gamma-Thio-GTP


  1. Dual ion-channel regulation by cyclic GMP and cyclic GMP-dependent protein kinase. Light, D.B., Corbin, J.D., Stanton, B.A. Nature (1990) [Pubmed]
  2. VAMP-2 and cellubrevin are expressed in pancreatic beta-cells and are essential for Ca(2+)-but not for GTP gamma S-induced insulin secretion. Regazzi, R., Wollheim, C.B., Lang, J., Theler, J.M., Rossetto, O., Montecucco, C., Sadoul, K., Weller, U., Palmer, M., Thorens, B. EMBO J. (1995) [Pubmed]
  3. Initiation by RNA polymerase II and formation of runoff transcripts containing unblocked and unmethylated 5' termini. Ernst, H., Filipowicz, W., Shatkin, A.J. Mol. Cell. Biol. (1983) [Pubmed]
  4. Augmentation of calcium channel currents in response to G protein activation by GTP gamma S in chick sensory neurons. Zong, X., Lux, H.D. J. Neurosci. (1994) [Pubmed]
  5. Nuclear phospholipase D in Madin-Darby canine kidney cells. Guanosine 5'-O-(thiotriphosphate)-stimulated activation is mediated by RhoA and is downstream of protein kinase C. Balboa, M.A., Insel, P.A. J. Biol. Chem. (1995) [Pubmed]
  6. Impaired G-protein-stimulated adenylyl cyclase activity in Alzheimer's disease brain is not accompanied by reduced cyclic-AMP-dependent protein kinase A activity. Bonkale, W.L., Fastbom, J., Wiehager, B., Ravid, R., Winblad, B., Cowburn, R.F. Brain Res. (1996) [Pubmed]
  7. The formation of Golgi stacks from vesiculated Golgi membranes requires two distinct fusion events. Acharya, U., Jacobs, R., Peters, J.M., Watson, N., Farquhar, M.G., Malhotra, V. Cell (1995) [Pubmed]
  8. The small GTP-binding protein Rho regulates a phosphatidylinositol 4-phosphate 5-kinase in mammalian cells. Chong, L.D., Traynor-Kaplan, A., Bokoch, G.M., Schwartz, M.A. Cell (1994) [Pubmed]
  9. ADP-ribosylation factor, a small GTP-dependent regulatory protein, stimulates phospholipase D activity. Brown, H.A., Gutowski, S., Moomaw, C.R., Slaughter, C., Sternweis, P.C. Cell (1993) [Pubmed]
  10. An essential role for phosphatidylinositol transfer protein in phospholipase C-mediated inositol lipid signaling. Thomas, G.M., Cunningham, E., Fensome, A., Ball, A., Totty, N.F., Truong, O., Hsuan, J.J., Cockcroft, S. Cell (1993) [Pubmed]
  11. Calcium mobilization is required for nuclear vesicle fusion in vitro: implications for membrane traffic and IP3 receptor function. Sullivan, K.M., Busa, W.B., Wilson, K.L. Cell (1993) [Pubmed]
  12. Differential regulation by cAMP-dependent protein kinase and protein kinase C of the mu opioid receptor coupling to a G protein-activated K+ channel. Chen, Y., Yu, L. J. Biol. Chem. (1994) [Pubmed]
  13. Pertussis toxin can activate human platelets. Comparative effects of holotoxin and its ADP-ribosylating S1 subunit. Banga, H.S., Walker, R.K., Winberry, L.K., Rittenhouse, S.E. J. Biol. Chem. (1987) [Pubmed]
  14. Angiotensin II and guanine nucleotides stimulate formation of inositol 1,4,5-trisphosphate and its metabolites in permeabilized adrenal glomerulosa cells. Baukal, A.J., Balla, T., Hunyady, L., Hausdorff, W., Guillemette, G., Catt, K.J. J. Biol. Chem. (1988) [Pubmed]
  15. Activation of a Gi protein in mouse sperm membranes by solubilized proteins of the zona pellucida, the egg's extracellular matrix. Ward, C.R., Storey, B.T., Kopf, G.S. J. Biol. Chem. (1992) [Pubmed]
  16. G protein-independent activation of an inward Na(+) current by muscarinic receptors in mouse pancreatic beta-cells. Rolland, J.F., Henquin, J.C., Gilon, P. J. Biol. Chem. (2002) [Pubmed]
  17. Involvement of GTP-binding "G" proteins in transport through the Golgi stack. Melançon, P., Glick, B.S., Malhotra, V., Weidman, P.J., Serafini, T., Gleason, M.L., Orci, L., Rothman, J.E. Cell (1987) [Pubmed]
  18. Tubular membrane invaginations coated by dynamin rings are induced by GTP-gamma S in nerve terminals. Takei, K., McPherson, P.S., Schmid, S.L., De Camilli, P. Nature (1995) [Pubmed]
  19. Exocytotic fusion is activated by Rab3a peptides. Oberhauser, A.F., Monck, J.R., Balch, W.E., Fernandez, J.M. Nature (1992) [Pubmed]
  20. A functional role for GTP-binding proteins in synaptic vesicle cycling. Hess, S.D., Doroshenko, P.A., Augustine, G.J. Science (1993) [Pubmed]
  21. Inactivation of a T cell receptor-associated GTP-binding protein by antibody-induced modulation of the T cell receptor/CD3 complex. Schrezenmeier, H., Ahnert-Hilger, G., Fleischer, B. J. Exp. Med. (1988) [Pubmed]
  22. Recruitment of coat proteins onto Golgi membranes in intact and permeabilized cells: effects of brefeldin A and G protein activators. Robinson, M.S., Kreis, T.E. Cell (1992) [Pubmed]
  23. Golgi membrane dynamics imaged by freeze-etch electron microscopy: views of different membrane coatings involved in tubulation versus vesiculation. Weidman, P., Roth, R., Heuser, J. Cell (1993) [Pubmed]
  24. Inhibition of an inwardly rectifying K+ channel by G-protein alpha-subunits. Schreibmayer, W., Dessauer, C.W., Vorobiov, D., Gilman, A.G., Lester, H.A., Davidson, N., Dascal, N. Nature (1996) [Pubmed]
  25. A pertussis toxin-sensitive G protein in hippocampal long-term potentiation. Goh, J.W., Pennefather, P.S. Science (1989) [Pubmed]
  26. GTP gamma S stimulates exocytosis in patch-clamped rat melanotrophs. Okano, K., Monck, J.R., Fernandez, J.M. Neuron (1993) [Pubmed]
  27. Enhanced G protein activation in immortalized lymphoblasts from patients with essential hypertension. Siffert, W., Rosskopf, D., Moritz, A., Wieland, T., Kaldenberg-Stasch, S., Kettler, N., Hartung, K., Beckmann, S., Jakobs, K.H. J. Clin. Invest. (1995) [Pubmed]
  28. Quisqualate receptor-mediated depression of calcium currents in hippocampal neurons. Lester, R.A., Jahr, C.E. Neuron (1990) [Pubmed]
  29. Thromboxane-insensitive dog platelets have impaired activation of phospholipase C due to receptor-linked G protein dysfunction. Johnson, G.J., Leis, L.A., Dunlop, P.C. J. Clin. Invest. (1993) [Pubmed]
  30. Alzheimer amyloid protein precursor complexes with brain GTP-binding protein G(o). Nishimoto, I., Okamoto, T., Matsuura, Y., Takahashi, S., Okamoto, T., Murayama, Y., Ogata, E. Nature (1993) [Pubmed]
  31. Inhibition of GTP hydrolysis by Sar1p causes accumulation of vesicles that are a functional intermediate of the ER-to-Golgi transport in yeast. Oka, T., Nakano, A. J. Cell Biol. (1994) [Pubmed]
  32. Regulation of cortical actin cytoskeleton assembly during polarized cell growth in budding yeast. Li, R., Zheng, Y., Drubin, D.G. J. Cell Biol. (1995) [Pubmed]
  33. Distinct biochemical requirements for the budding, targeting, and fusion of ER-derived transport vesicles. Rexach, M.F., Schekman, R.W. J. Cell Biol. (1991) [Pubmed]
  34. Low molecular weight GTP-binding proteins in HL-60 granulocytes. Assessment of the role of ARF and of a 50-kDa cytosolic protein in phospholipase D activation. Bourgoin, S., Harbour, D., Desmarais, Y., Takai, Y., Beaulieu, A. J. Biol. Chem. (1995) [Pubmed]
  35. Cholera toxin elevates pathogen resistance and induces pathogenesis-related gene expression in tobacco. Beffa, R., Szell, M., Meuwly, P., Pay, A., Vögeli-Lange, R., Métraux, J.P., Neuhaus, G., Meins, F., Nagy, F. EMBO J. (1995) [Pubmed]
  36. Activation of pigeon erythrocyte membrane adenylate cyclase by guanylnucleotide analogues and separation of a nucleotide binding protein. Pfeuffer, T., Helmreich, E.J. J. Biol. Chem. (1975) [Pubmed]
  37. Purification and identification of FOAD-II, a cytosolic protein that regulates secretion in streptolysin-O permeabilized mast cells, as a rac/rhoGDI complex. O'Sullivan, A.J., Brown, A.M., Freeman, H.N., Gomperts, B.D. Mol. Biol. Cell (1996) [Pubmed]
  38. A site on transducin alpha-subunit of interaction with the polycationic region of cGMP phosphodiesterase inhibitory subunit. Artemyev, N.O., Mills, J.S., Thornburg, K.R., Knapp, D.R., Schey, K.L., Hamm, H.E. J. Biol. Chem. (1993) [Pubmed]
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