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Chemical Compound Review

HSDB 600     trifluoroalumane

Synonyms: CCRIS 2282, CHEBI:49464, LS-2205, CBiol_002057, CPD0-1229, ...
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Disease relevance of trifluoroalumane

  • Although modulation of T-type currents is membrane-delimited, it was not affected by GDP-beta-S (2 mM), GTP-gamma-S (200 microM), 5'-guanylyl-imidodiphosphate tetralithium (200 microM), aluminum fluoride (AlF4-, 100 microM), or pertussis toxin, suggesting that a GTP-insensitive pathway was involved [1].
  • Mechanisms of aluminum fluoride- and insulin-stimulated p33 mRNA accumulation in rat hepatoma cells: involvement of a G protein and kinase action and demonstration of effects on mRNA turnover [2].
  • Treatment with Clostridium difficile toxin B blocked PKD3 activation induced by either bombesin or by aluminum fluoride-stimulated Galpha(12/13) but did not affect Galpha(q)-induced PKD3 activation [3].
  • No differences were found between the body weights of rats in the different treatment groups although more rats died in the AlF3 group than in the control group [4].
  • The structure of the very strong solid Lewis acid aluminum chlorofluoride (ACF, AlCl(x)F(3-x), x = 0.05-0.3) was studied by IR, ESR, Cl K XANES, (19)F MAS NMR, and (27)Al SATRAS NMR spectroscopic methods and compared with amorphous aluminum fluoride conventionally prepared by dehydration of alpha-AlF(3) x 3H(2)O [5].

Psychiatry related information on trifluoroalumane

  • In subsequent experiments, basal and guanosine 5'-O-(3-thiotriphosphate)-, aluminum fluoride-, and forskolin-stimulated enzyme activities were compared in five brain regions from a series of eight Alzheimer's disease and seven matched nondemented control subjects [6].

High impact information on trifluoroalumane

  • Removal of 80% of GGBFs from cytosol abolishes GTP gamma S sensitivity but does not affect inhibition by aluminum fluoride [7].
  • Early vesicle fusion events that follow receptor-mediated endocytosis as measured by three in vitro assays were blocked by guanosine 5'-O-(3-thiotriphosphate) and aluminum fluoride [8].
  • Dose responses to a G-protein activator, aluminum fluoride, were again not different between these two groups [9].
  • Aluminum fluoride (AlF) treatment of ARF6-transfected cells redistributes ARF6 to the PM and stimulates the formation of actin-rich surface protrusions [10].
  • Whereas AlF treatment blocked internalization, CD treatment blocked the recycling of wild-type ARF6 and Tac back to the PM; these blocks were mimicked by expression of ARF6 mutants Q67L and T27N, which were predicted to be in either the GTP- or GDP-bound state, respectively [10].

Chemical compound and disease context of trifluoroalumane


Biological context of trifluoroalumane


Anatomical context of trifluoroalumane

  • Previously shown to indirectly activate the ARF1 GTPase, aluminum fluoride (AIF) treatment of ARF6-transfected cells resulted in a redistribution of both ARF6 and actin to discrete sites on the plasma membrane, which became increasingly protrusive over time [21].
  • Incubation with aluminum fluoride resulted in fragmentation of the Golgi complex into large clusters of beta-COP positive vesicles, while 50% of the label remained in the cytoplasm, as in control cells [22].
  • Aluminum fluoride, a general activator of heterotrimeric G proteins, inhibited the transport of the basolateral cognate proteins, as well as of the hemagglutinin mutant, from the TGN to the cell surface in BHK and CHO cells, while having no effect on the surface delivery of the wild-type hemagglutinin [23].
  • In the presence of GTP, aluminum fluoride, an activator of trimeric G proteins, promotes the stable ARF-dependent binding of coatomer to membranes, even though this reagent does not itself activate ARF [24].
  • Beryllium fluoride and aluminum fluoride also reduce this rate, and they increase the affinity of kinesin for microtubules [25].

Associations of trifluoroalumane with other chemical compounds


Gene context of trifluoroalumane

  • Here we show that cytochalasin D (CD) treatment inhibited formation of the AlF-induced protrusions and shifted the distribution of ARF6 to a tubular membrane compartment emanating from the juxtanuclear region of cells, which resembled the compartment where the GTP-binding defective mutant of ARF6 localized [10].
  • These two mutants had a dominant-negative effect, preventing endogenous wild-type hGBP-1 from efficiently redistributing after aluminum fluoride treatment [31].
  • Different inhibitory potencies of RGS2 were observed under conditions assessing its activity as a GAP versus as an effector antagonist; i.e. RGS2 was a 10-20-fold more potent inhibitor of aluminum fluoride and GTP-stimulated PLC-betat activity than of GTPgammaS-promoted PLC-betat activity [32].
  • Cells expressing wild-type ARF6 or Rac1 formed actin-containing surface protrusions and membrane ruffles, respectively, upon treatment with the G protein activator aluminum fluoride [33].
  • Treatment with protein kinase C (PKC) inhibitors prevented the increase in PKD3 activity induced by RacV12 and aluminum fluoride-stimulated Galpha(12/13) [3].

Analytical, diagnostic and therapeutic context of trifluoroalumane


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  17. Crystal structure of a transition state mimic of the catalytic subunit of cAMP-dependent protein kinase. Madhusudan, n.u.l.l., Akamine, P., Xuong, N.H., Taylor, S.S. Nat. Struct. Biol. (2002) [Pubmed]
  18. Stimulation of PIP2 hydrolysis by aluminum fluoride in resting T cell subsets of normal and autoimmune-prone lpr mice. Coggeshall, K.M., Altman, A. J. Immunol. (1989) [Pubmed]
  19. Binding of phosphate, aluminum fluoride, or beryllium fluoride to F-actin inhibits severing by gelsolin. Allen, P.G., Laham, L.E., Way, M., Janmey, P.A. J. Biol. Chem. (1996) [Pubmed]
  20. Determinants of gi1alpha and beta gamma binding. Measuring high affinity interactions in a lipid environment using flow cytometry. Sarvazyan, N.A., Remmers, A.E., Neubig, R.R. J. Biol. Chem. (1998) [Pubmed]
  21. Aluminum fluoride stimulates surface protrusions in cells overexpressing the ARF6 GTPase. Radhakrishna, H., Klausner, R.D., Donaldson, J.G. J. Cell Biol. (1996) [Pubmed]
  22. Beta-COP localizes mainly to the cis-Golgi side in exocrine pancreas. Oprins, A., Duden, R., Kreis, T.E., Geuze, H.J., Slot, J.W. J. Cell Biol. (1993) [Pubmed]
  23. Different biosynthetic transport routes to the plasma membrane in BHK and CHO cells. Yoshimori, T., Keller, P., Roth, M.G., Simons, K. J. Cell Biol. (1996) [Pubmed]
  24. Aluminum fluoride acts on the reversibility of ARF1-dependent coat protein binding to Golgi membranes. Finazzi, D., Cassel, D., Donaldson, J.G., Klausner, R.D. J. Biol. Chem. (1994) [Pubmed]
  25. Equilibrium studies of kinesin-nucleotide intermediates. Rosenfeld, S.S., Rener, B., Correia, J.J., Mayo, M.S., Cheung, H.C. J. Biol. Chem. (1996) [Pubmed]
  26. A mutation in the heterotrimeric stimulatory guanine nucleotide binding protein alpha-subunit with impaired receptor-mediated activation because of elevated GTPase activity. Warner, D.R., Weinstein, L.S. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  27. Transmembrane signaling in human polymorphonuclear neutrophils: 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid modulates receptor agonist-triggered cell activation. Smith, R.J., Justen, J.M., Nidy, E.G., Sam, L.M., Bleasdale, J.E. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  28. Muscarine and t-LHRH suppress M-current by activating an IAP-insensitive G-protein. Pfaffinger, P. J. Neurosci. (1988) [Pubmed]
  29. Inositol trisphosphate production in squid photoreceptors. Activation by light, aluminum fluoride, and guanine nucleotides. Wood, S.F., Szuts, E.Z., Fein, A. J. Biol. Chem. (1989) [Pubmed]
  30. The role of tyrosine phosphorylation in signal transduction through surface Ig in human B cells. Inhibition of tyrosine phosphorylation prevents intracellular calcium release. Lane, P.J., Ledbetter, J.A., McConnell, F.M., Draves, K., Deans, J., Schieven, G.L., Clark, E.A. J. Immunol. (1991) [Pubmed]
  31. Golgi targeting of human guanylate-binding protein-1 requires nucleotide binding, isoprenylation, and an IFN-gamma-inducible cofactor. Modiano, N., Lu, Y.E., Cresswell, P. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  32. Protein kinase C phosphorylates RGS2 and modulates its capacity for negative regulation of Galpha 11 signaling. Cunningham, M.L., Waldo, G.L., Hollinger, S., Hepler, J.R., Harden, T.K. J. Biol. Chem. (2001) [Pubmed]
  33. ARF6 requirement for Rac ruffling suggests a role for membrane trafficking in cortical actin rearrangements. Radhakrishna, H., Al-Awar, O., Khachikian, Z., Donaldson, J.G. J. Cell. Sci. (1999) [Pubmed]
  34. A point mutation in Galphao and Galphai1 blocks interaction with regulator of G protein signaling proteins. Lan, K.L., Sarvazyan, N.A., Taussig, R., Mackenzie, R.G., DiBello, P.R., Dohlman, H.G., Neubig, R.R. J. Biol. Chem. (1998) [Pubmed]
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