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

• Pretreatment of cells with pertussis toxin (0.1 microgram/ml for 12-13 h) prevented this current's induction both by guanine nucleotides and aluminum fluoride, but had no effect on the decrease in inward rectifier conductance [11].
• Other activators of G-proteins, including the tetradecapeptide mastoparan, pertussis toxin and AlF3, also caused no significant release of membrane dipeptidase from the surface of the 3T3-L1 adipocytes [12].
• In addition, melatonin can facilitate secretion via a cholera and pertussis toxins-insensitive mechanism which can be inhibited by aluminum fluoride [13].
• Cholera and pertussis toxins, as well as aluminum fluoride, also potentiated the release of prostacyclin induced by ionophore A23187 [14].
• NaF and AlF3 each significantly stimulated the proliferation of human TE85 osteosarcoma cells, increased cellular alkaline phosphatase (ALP) activity, and increased MAPK tyrosine phosphorylation level [15].

Biological context of trifluoroalumane

• Tyrphostin had no effect on the capacity of aluminum fluoride to increase [Ca2+]i. To determine whether a function of PTK is the phosphorylation of PLC, immunoprecipitates obtained with anti-phosphotyrosine from detergent lysates of B-lymphoblastoid cells were assayed for PLC activity [16].
• To understand the molecular mechanism underlying phosphoryl transfer of cAMP-dependent protein kinase, the structure of the catalytic subunit in complex with ADP, aluminum fluoride, Mg2+ ions and a substrate peptide was determined at 2.0 A resolution [17].
• Stimulation of PIP2 hydrolysis by aluminum fluoride in resting T cell subsets of normal and autoimmune-prone lpr mice [18].
• Our data suggest that they are sequentially occupied following ATP hydrolysis by HPO4(2-) which is subsequently titrated to H2PO4-. We speculate that beryllium fluoride and aluminum fluoride bind to the HPO4(2-) binding site [19].
• The kinetics of aluminum fluoride-stimulated dissociation were slower than those of the alpha subunit conformational change detected by intrinsic fluorescence [20].

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

• It has been reported that substitution of Arg258, a residue within the GTPase domain of the heterotrimeric guanine nucleotide binding protein (G protein) alpha-subunit (alphas), to alanine (alphas-R258A) results in decreased activation by receptor or aluminum fluoride (AlF4-) and increased basal GDP release [26].
• 15-HETE suppressed O2- production and increases in intracellular [Ca2+] induced when cell-surface receptors were bypassed and the PMN were activated directly by the guanine nucleotide-binding protein (G protein) activators aluminum fluoride (AlF4-) and mastoparan [27].
• Dialysis of cells with the G-protein activators GTP gamma S, fluoride, and aluminum fluoride causes loss of M-current [28].
• Inositol trisphosphate production in squid photoreceptors. Activation by light, aluminum fluoride, and guanine nucleotides [29].
• Herbimycin- and genistein-treated lymphocytes are nevertheless still capable of responding to aluminum fluoride with a rise in intracellular calcium [30].

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

• Redistribution from the cytosol to the Golgi was observed by immunofluorescence and subcellular fractionation after aluminum fluoride treatment, suggesting that it occurs when hGBP-1 is in its GTP-bound state [31].
• Quantitative flow cytometry binding studies show IC50 values of 30 and 96 nM, respectively, for aluminum fluoride-activated wild type alphao and alphai1 to compete with fluorescein isothiocyanate-alphao binding to glutathione S-transferase-RGS4 [34].
• The aluminum fluoride complexes were estimated by combining the data of the free and total fluoride determined using a fluoride ion-selective electrode, with the assumption that 2+ charged aluminum species consisted only of AlF2+ [35].
• PbF2 compared to Al2O3 and AlF3 to produce an epithermal neutron beam for radiotherapy [36].
• Epithermal neutron beams shaped by three moderator materials, Al/AlF3, 7LiF, and D2O, have been analyzed and their usefulness for boron neutron capture therapy (BNCT) treatments evaluated [37].

References