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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of fluorescent ATP analog 2'(3')-O-[N-[2-[3-(5-fluoresceinyl)thioureido]-ethyl]carbamoyl]adenosine 5'-triphosphate (FEDA-ATP) with rabbit skeletal myosin subfragment 1 (S1) and acto-S1 was studied. This and related ATP analogs are potentially useful for determination of the ATPase activity of single myosin filaments using fluorescence microscopy [Sowerby et al. (1993) J. Mol. Biol. 234, 114-123]. However, it is necessary that such analogs mimic ATP in their kinetics of turnover. The apparent second-order association rate constants for FEDA-ATP binding to S1 and for FEDA-ATP-induced dissociation of acto-S1 are about 4 times slower than those for ATP. As with ATP, the hydrolysis step is fast, so that the M.FEDA-ADP.P(i) complex is the major steady-state intermediate. The turnover rate is the same for the 2' and 3' FEDA-ATP derivatives and similar to that of ATP itself. The dissociation rate constant for FEDA-ADP from S1 is identical to that for ADP. Actin-activated turnover is comparable for both FEDA-ATP and ATP. The corresponding rhodamine and sulfoindocyanine, Cy3.18 (Cy3), derivatives also appear to be reasonable analogs. FEDA-ATP binding leads to a 25-40% reduction in fluorescein fluorescence. Spectral properties of the bound nucleotide were explored by trapping FEDA-ADP as its aluminum fluoride complex. The fluorescence quenching is a consequence of a reduction in both absorbance and excited-state lifetime, but there is little change in spectral shape.
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PMID:Kinetic and spectroscopic characterization of fluorescent ribose-modified ATP analogs upon interaction with skeletal muscle myosin subfragment 1. 865 70

The aim of this study was to highlight a possible new non-aluminum phosphate-binder to limit hyperphosphatemia in patients with renal failure. Lanthanum chloride hydrate was evaluated as a dietary phosphate binder in rats. Aluminum chloride hexahydrate was evaluated as a reference. Animals were divided in five groups (6 animals per group): 1 control group (C), 2 aluminum groups (Al1 and Al2), receiving different doses of aluminum chloride hexahydrate and 2 lanthanum groups (La1 and La2), receiving different doses of lanthanum chloride hydrate. During the treatment, urine and stools were collected. At the end of the treatment animals were sacrificed and plasma and different organs were collected (liver, spleen, kidneys, brain and femur). To highlight the possible transfer of lanthanum in rat tissues, a long-term (100 days) study was carried with a high dose. At the end of the treatment, lanthanum determinations were carried out on several tissues (liver, spleen, kidneys, brain, femur and lungs). Determinations of phosphorus and calcium levels in plasma indicated that lanthanum chloride hydrate showed as good results as aluminum chloride hexahydrate. Lanthanum chloride hydrate significantly (p < 0.01) reduced the bone phosphorus burden. Decreases of urinary excretion and increases in fecal excretion of phosphorus indicated a severe phosphorus depletion in all treatments (Al and La). Unfortunately, in the long-term study, lanthanum traces could only be determined in the different tissues but not in plasma. However, in comparison with the equivalent aluminum treatment, the transfer of lanthanum was less important than aluminum transfer. Consequently, lanthanum could provide a possible alternative to aluminum.
Res Commun Mol Pathol Pharmacol 1995 Sep
PMID:A possible non-aluminum oral phosphate binder? A comparative study on dietary phosphorus absorption. 868 Aug 6

The effects of aluminum and other metal ions on the synthesis of nerve growth factor (NGF) by cultured mouse brain astroglial cells have been investigated. Natural NGF formation was dependent on the AlCl3 concentration of the cell culture medium; it was stimulated at low concentrations but was inhibited at higher concentrations. Catechol-stimulated NGF formation was also inhibited at AlCl3/catechol molar ratios > 0.3, whereas ZnCl2 and CaCl2 had no effect under similar conditions. Ethylenediamine-N,N,N',N'-tetraacetate (EDTA) and citrate blocked the inhibitory effect of Al(III). These observations were explained by the complex formation between Al(III) and catechols.
Biochem Mol Biol Int 1996 Apr
PMID:Effects of aluminum(III) on catechol-stimulated nerve growth factor biosynthesis by cultured mouse brain astroglial cells. 872 96

The aim of this study was to study a possible new non-aluminum phosphate-binder to limit hyperphosphatemia in patients with renal failure. Zirconyl chloride octahydrate was evaluated as a dietary phosphate binder in rats. Aluminum chloride hexahydrate was used as a reference. Animals were divided into six groups (6 animals per group): One - control group (C), two - aluminum groups (Al1 and Al2) and three - zirconium groups (Zr1, Zr2 and Zr3) receiving different doses of zirconyl chloride octahydrate. Urines were collected during the experimental period. At the end of the treatment, the animals were sacrified and plasma and different organs were collected (liver, spleen, kidneys, brain and femur). Determination of phosphorus and calcium levels in plasma indicated that zirconyl chloride octahydrate yielded as good results as aluminum chloride hexahydrate did. Zirconyl chloride octahydrate significantly (p<0.01) reduced bone phosphorus burden. Urinary excretion of phosphorus indicated a severe phosphorus depletion in all treatments. Not even traces of zirconium could be determined in the different tissues, in urines or in plasma. Consequently, it is important to carry out experiments with zirconium compounds in order to develop non-aluminum-containing phosphate binders.
Res Commun Mol Pathol Pharmacol 1995 Dec
PMID:Reduction of dietary phosphorus absorption by oral phoshorus binders. 874 85

As observed for neurons in situ, phosphorylated neurofilament (NF) epitopes are normally segregated within the axonal cytoskeleton of NB2a/d1 cells. However, accumulations of phosphorylated NFs develop in NB2a/d1 perikarya following exposure to aluminum salts and following inhibition of proteolysis. In the present study, we observed that perikarya of cells exposed to both aluminum and the protease inhibitor C1 (also known as "AllNal") were more intensely labeled by monoclonal antibodies directed against both nonphosphorylated and phosphorylated epitopes than were cells treated with either aluminum or protease inhibitor alone. Since these monoclonal antibodies crossreact with tau, we also immunostained cells treated under these conditions with monoclonal antibodies directed against phosphate-insensitive (5E2) and phosphorylated (PHF-1) epitopes of tau. Aluminum treatment, but not C1 treatment, induced accumulation of total tau isoforms as judged by an increase in 5E2 immunoreactivity. Neither treatment, either separately or in combination, induced an increase in PHF-1 immunoreactivity. These findings suggest that alterations in immunoreactivity with SMI antibodies reflected increases in NF epitopes. This was confirmed by immunoblot analyses. Since proteolysis is apparently instrumental in maintaining the normal distribution patterns of phosphorylated NF epitopes, these findings implicate deficiencies in proteolytic mechanisms in the development of neurofibrillary pathology, and underscore the possibility of a multiple etiology in human neuropathological conditions.
Mol Chem Neuropathol 1995 Dec
PMID:Inhibition of proteolysis enhances aluminum-induced perikaryal neurofilament accumulation but does not enhance tau accumulation. 874 24

Aluminum, responsible of dialysis encephalopathy, is suspected to be involved in other neurological disorders such as Alzheimer disease. Absorption of aluminum from the digestive tract can be enhanced by the concommittant intake of substances such as citrate. We studied in rats and mice the interactions between fluoride and aluminum for their digestive absorption and showed that fluoride increased the levels of aluminum in plasma as much as citrate whereas aluminum decreased the absorption of fluoride. This result could be the consequence of the high affinity between aluminum and fluoride which form complexes able to increase the absorption of aluminum and to decrease the absorption of fluoride.
Res Commun Mol Pathol Pharmacol 1996 Feb
PMID:Enhancement of aluminum digestive absorption by fluoride in rats. 883 14

Aluminum is suspected to play a role in several neurological disorders. Reactive oxygen species (ROS) lead to oxidative stress, which is thought to be a possible mechanism for neurological damage. Interactions between aluminum and iron, a known promoter of prooxidant events, were studied in cerebral tissues using a fluorescent probe to measure rates of generation of ROS. Al2(SO4)3 alone failed to stimulate ROS production over a wide range of concentrations (50-1000 microM). The aluminum-deferrioxamine chelate in the absence of iron could also not potentiate ROS formation. However, Al2(SO4)3 potentiated FeSO4-induced ROS, with a maximal effect at 10 microM Fe and 500 microM Al. Kaolin, a hydrated aluminum silicate, did not potentiate iron-induced ROS formation. Ferritin had a minor stimulatory effect on ROS generation, but this was not potentiated by the concurrent presence of Al2(SO4)3. Transferrin had no effect on basal rates of ROS generation, but when Al2(SO4)3 was also present, ROS production was enhanced. It is concluded that: 1. There is a potentiation of iron-induced ROS by aluminum salts; 2. Free or complexed aluminum alone is not a key producer of ROS; and 3. High rates of ROS production are unlikely to be owing to the displacement by aluminum iron from its biologically sequestered locations.
Mol Chem Neuropathol 1996 Feb
PMID:The promotion of iron-induced generation of reactive oxygen species in nerve tissue by aluminum. 896 2

Results of the present study suggest that aluminum treatment to rats resulted in elevation of microsomal lipid peroxidation along with inhibition of catalase activity in the liver. Aluminum treatment to rats has no significant effect on rat liver superoxide dismutase activity. A 25% inhibition in catalase activity was observed when liver supernatant was incubated with A1C13 at 5 x 10(-3) M concentration and above.
Res Commun Mol Pathol Pharmacol 1996 Nov
PMID:Effect of aluminum on superoxide dismutase, catalase and lipid peroxidation of rat liver. 898 19

The present study investigates the possible effects of chronic aluminium exposure on the various aspects of calcium homeostasis in the primate central nervous system. Aluminium administration caused a marked decline in the activity of Ca2+ ATPase in the monkey brain. The total calcium content was also significantly raised following aluminium exposure. Concomittant to the increase in the calcium content, the levels of lipid peroxidation were also augmented in the aluminium treated animals, thereby further accentuating the aluminium induced neuronal damage. In addition, aluminium had an inhibitory effect on the depolarization induced 45Ca2+ uptake via the voltage operated channels. The results presented herein, indicate that the toxic effects of aluminium could be mediated through modifications in the intracellular calcium homeostasis with resultant altered neuronal function.
Mol Cell Biochem 1997 Mar
PMID:Regional alterations in calcium homeostasis in the primate brain following chronic aluminium exposure. 906 98

We are developing budding yeast, Saccharomyces cerevisiae, as a genetic system for the study of tolerance to the trivalent aluminum cation (Al3+). We have isolated eight mutants that are more sensitive to Al3+ than the wild type. Each mutant represented a different complementation group. A number of the mutants were pleiotropic, and showed defects in other stress responses, changes in tolerance to other metal cations, or abnormal morphology. Two mutants also showed increased dependence on supplemental Mg2+ and Ca2+. One mutant with a relatively specific sensitivity to Al3+ was chosen for molecular complementation. Normal Al3+ tolerance was restored by expression of the MAP kinase gene SLT2. Strains carrying deletions of the SLT2 gene, or of the gene for the corresponding MAP kinase kinase SLK1, showed sensitivity to Al3+. These results indicate that the SLT2 MAP kinase signal transduction pathway is required for yeast to sense and respond to Al3+ stress.
Mol Gen Genet 1997 Mar 18
PMID:Aluminum-sensitive mutants of Saccharomyces cerevisiae. 910 91


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