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Sökning: L773:0361 7742

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  • Arner, Anders, et al. (författare)
  • Influence of ATP, ADP and AMPPNP on the energetics of contraction in skinned smooth muscle
  • 1987
  • Ingår i: Progress in Clinical and Biological Research. - 0361-7742. ; 245, s. 43-57
  • Tidskriftsartikel (refereegranskat)abstract
    • The contraction of smooth muscle is influenced by the substrate MgATP and the product MgADP. The effects on force, shortening velocity and ATP-turnover, are consistent with an influence on the kinetics of cross-bridge cycling. Part of these effects are mediated via an influence on the regulation of contraction by myosin light chain phosphorylation. Results from preparations activated by thiophosphorylation, show that MgATP and MgADP also interact directly at the cross-bridge level, and are consistent with MgADP acting as a competitive ATP-analogue. The slow shortening velocity and decreased rate of ATP-induced relaxation from rigor in the presence of MgADP, suggest an inhibition of cross-bridge detachment. The rate of ATP-turnover was decreased in the presence of the nonhydrolyzable ATP-analogue AMPPNP. These results may contribute to the characterization of the biochemical reactions in the structurally organized smooth muscle contractile system. In addition, the influence of MgATP and MgADP on smooth muscle contraction suggest that the concentrations of substrate and products, at the level of the contractile proteins, may constitute important regulatory factors in vivo under conditions, such as hypoxia and ischemia, associated with impaired cellular energy supply.
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  • Hellstrand, Per, et al. (författare)
  • Mechanical transients in smooth muscle
  • 1989
  • Ingår i: Progress in Clinical and Biological Research. - 0361-7742. ; 315, s. 347-357
  • Tidskriftsartikel (refereegranskat)
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  • Palsdottir, A, et al. (författare)
  • Mutation in the cystatin C gene causes hereditary brain hemorrhage
  • 1989
  • Ingår i: Progress in Clinical and Biological Research. - 0361-7742. ; 317, s. 241-246
  • Tidskriftsartikel (refereegranskat)abstract
    • Hereditary cystatin C amyloid angiopathy (HCCAA) is an autosomal dominant disorder leading to massive brain hemorrhage and death in young adults (Jensson et al., 1987). A variant of a potent inhibitor of cysteine proteinases, cystatin C (Barrett et al., 1984), is deposited as amyloid fibrils in the cerebral arteries of the patients (Ghiso et al., 1986). We have used the full length cystatin C cDNA probe (Abrahamson et al., 1987) to demonstrate a mutation in the codon for leucine at position 68, which abolishes an Alu I restriction site in cystatin C gene of the HCCAA patients. The Alu I marker has been used to show that this mutation is transmitted only in the affected members in all eight families investigated, proving that the mutated cystatin C gene causes HCCAA. This DNA marker will be useful for the diagnosis of HCCAA in patients, asymptomatic affected individuals and also for pre-natal diagnosis. HCCAA is the first human disorder known to be caused by an abnormal gene for a cysteine proteinase inhibitor
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