Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of retraction of the longitudinal flagellum of Ceratium tripos was studied by making extracted models of the flagellum. Non-detergent models extracted in low ionic strength medium containing 1 M-glucose, 10 mM-EDTA, and 50 mM-Tris X HCl buffer (pH 8.0), retracted when Ca2+, Mg2+, Ba2+, Sr2+, Mn2+ or Cd2+ was applied locally with a glass capillary. A demembranated model of the flagellum was made with an extraction medium containing 0.8-1.0 M-glucose, 20 mM-Tris-acetate (pH 7.8), 2 mM-EGTA, 5-7 mM-MgSO4, 0.1 M-potassium glutamate and 0.1% Triton X-100. The model required a concentration of Mg2+ of a few mmol/l for successful reactivation of both retraction and undulation, and about 0.1 M-potassium glutamate (or sodium glutamate) for reactivation of undulation. Neither type of motion of the models could be reactivated above 35 degrees C. Ca2+ induced the retraction at pCa 5.5 or less. In addition to Ca2+, Mn2+, Ba2+, Sr2+ and Cd2+ also induced retraction but Mg2+, La3+ or Tb3+ did not. Although ATP was required for undulation, it was not required for retraction. Co-incubation with hexokinase to remove contaminating ATP did not suppress the retraction. The potent ATPase inhibitor, orthovanadate, inhibited undulation at 10 micron but did not inhibit retraction even at 2 mM. SH blockers, N-ethylmaleimide and dithio-bis-nitrobenzoic acid strongly suppressed undulation but had no effect on retraction. Calmodulin inhibitors, trifluoperazine and chlorpromazine, also had no effect on retraction. These data indicate that undulation is generated by a 9 + 2 microtubular axoneme using energy released by hydrolysis of ATP and that retraction can be induced by Ca2+ without a requirement for ATP.
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PMID:Extraction model of the longitudinal flagellum of Ceratium tripos (Dinoflagellida): reactivation of flagellar retraction. 385 92

The Na/K pump in human red blood cells that normally exchanges 3 Nai for 2 Ko is known to continue to transport Na in a ouabain-sensitive and ATP-dependent manner when the medium is made free of both Nao and Ko. Although this Na efflux is called "uncoupled" because of removal of ions to exchange with, the efflux has been shown to be comprised of a coefflux with cellular anions. The work described in this paper presents a new mode of operation of uncoupled Na efflux. This new mode not only depends upon the combined presence of ADP and intracellular orthophosphate (P(i))i but the Na efflux that is stimulated to occur is coeffluxed with (P(i))i. These studies were carried out with DIDS-treated resealed red cell ghosts, suspended in buffered (NMG)2SO4, that were made to contain, in addition to other constituents, varying concentrations of ADP and P(i) together with Na2 SO4, MgSO4 and hexokinase. While neither ADP nor P(i) was effective alone, ouabain-sensitive uncoupled Na efflux, (measured with 22Na) could be activated by [ADP+P(i)] where the K0.5 for ADP in the presence of 10 mmol (P(i))i/liter ghosts was 100-200 mumol/liter ghosts and the K0.5 for (P(i))i, in the presence of 500 mumol ADP/liter ghosts was 3-4 mmol/liter ghosts. [ADP+P(i)] activation of this Na efflux could be inhibited by as little as 2 mumol ATP/liter ghosts but the inhibition could be relieved by the addition of 50 mM glucose, given entrapped hexokinase. While ouabain-sensitive Na efflux was found to be coeffluxed with P(i) (measured with entrapped [32P]H3PO4), this was not so for SO4 (measured with 35SO4). The stoichiometry of Na to P(i) efflux was found to be approximately 2 to 1. Na efflux as well as (P(i))i efflux were both inhibited by 10 mM Nao (K0.5 approximately equal to 4 mM). But, whereas 20 mM Ko (K0.5 approximately equal to 6 mM) inhibited the efflux of (P(i))i, as would be expected from previous work, Na efflux was actually increased. When Ko influx was measured in this situation there was a 1 for 1 exchange of Nai for Ko, that is, of course, downhill with respect to the gradient of each ion. Surprisingly AsO4 was unable to replace P(i) for activation of Na efflux but Na efflux could be inhibited by vanadate and oligomycin. In terms of mechanism, it is likely that ADP acts to promote the formation of the phosphoenzyme (EP) by (P(i))i that would otherwise be inhibited by Nai.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:ADP+orthophosphate (P(i)) stimulates an Na/K pump-mediated coefflux of P(i) and Na in human red blood cell ghosts. 796 95