Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Muscle evidence for

Spach MS, Dolber PC Relating extracellular potentials and their derivatives to anisotropic propagation at a microscopic level in human cardiac muscle. Evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ Res 1986 58 356-371. [Pg.136]

Spach MS, Miller WT III, Geselowitz DB, Barr RC, Kootsey JM, Johnson EA The discontinuous nature of propagation in normal canine cardiac muscle Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981 48 39 15. [Pg.136]

Harford, J. J., Chew, M. W., Squire, J. M., and Towns-Andrews, E. (1991). Crossbridge states in isometrically contracting fish muscle Evidence for swinging of myosin heads on actin. Adv. Biophys. 27, 45-61. [Pg.249]

Guma, A., Testar, X., Palacin, M., Zorzano, A. (1988). Insulin-stimulated a-(methyl) aminoisobutyric acid uptake in skeletal muscle. Evidence for a short-term activation of uptake independent of Na+-electrochemical gradient and protein synthesis. Biochem. J. 253, 625-629. [Pg.116]

H62. Hussey, A. J., Kerr, L. A., Cronshaw, A. D., Harrison, D. J., and Hayes, J. D., Variation in the expression of mu-class glutathione S-transferase isoenzymes from human skeletal muscle Evidence for the existence of heterodimers. Biochem. J. 273, 323-332 (1991). [Pg.369]

Ikebe M, Brozovich FV (1996) Protein kinase C increases force and slows relaxation in smooth muscle evidence for regulation of the myosin light chain phosphatase. Biochem Biophys Res Commun 225 370-376 Ikebe M, Reardon S (1989) Location of the inhibitory region of smooth muscle myosin light chain kinase. J. Biol Chem 264 6967-6971 Ishizaki T, Maekawa M, Fujisawa K, Okawa K, Iwamatsu A, Fujita A, Watanabe N, Saito Y, Kakizuka A, Morri N, Narumiya S. (1996) The small GTP-binding protein Rho binds to and activates a 160 kDa Ser/Thr protein kinase homologous to myotonic dystrophy kinase. EMBO J 15 1885-1893... [Pg.228]

Fructose bisphosphate aldolase of animal muscle is a Class I aldolase, which forms a Schiff base or imme intermediate between the substrate (fructose-1,6-bisP or dihydroxyacetone-P) and a lysine amino group at the enzyme active site. The chemical evidence for this intermediate comes from studies with the aldolase and the reducing agent sodium borohydride, NaBH4. Incubation of fructose bisphosphate aldolase with dihydroxyacetone-P and NaBH4 inactivates the enzyme. Interestingly, no inactivation is observed if NaBH4 is added to the enzyme in the absence of substrate. [Pg.622]

In rat liver mitochondria, in state 4, the AP was estimated to be about 220 mV, with the membrane potential representing about 90% of this (Nicholls, 1974 Appendix 3). Similar values have been reported for human and rat skeletal muscle mitochondria in state 4 (Stumpf et al., 1982). The control of the rate of electron transport is not only determined by the availability of ADP, but also of Pj oxidizable substrates, and oxygen. There is evidence for futile cycling of protons in intact normal rat hepatocytes (Brand et al., 1993). Recently, Porter and Brand (1993) found a correlation between the proton permeability of the inner membrane of liver mitochondria and body size in animals from the mouse (20 g) to horses (150 kg) with a decrease in permeability with increasing weight of several-fold at a constant... [Pg.136]

Brenner, B.M., Yu, L.C., Podolsky, R.J. (1984). X-ray evidence for crossbridge formation in relaxed muscle fibers at various ionic strengths. Biophys. J. 46,299-306. [Pg.235]

Furthermore, it has been found that ouabain, convallatoxin, and cymarin inhibit the PTX-induced contraction of rabbit aortic vascular smooth muscle (79). These observations have also provided evidence for the involvement of Na ,K -ATPase on the contractile effect of PTX in smooth muscle. [Pg.222]

Free-radical species have been implicated in the pathogenesis of both muscle fatigue and muscle damage, and the evidence for these will be discussed separately. [Pg.176]

Kayano, T., et al. Evidence for a family of human glucose transporterlike proteins. Sequence and gene localization of a protein expressed in fetal skeletal muscle and other tissues. J. Biol. Chem. 1988, 263, 15245-15248. [Pg.282]

H., Gottesman, M. M., Pastan, I., Willingham, M. C., Immunohisto-chemical localization in normal tissues of different epitopes in the multidrug transport protein PI70 evidence for localization in brain capillaries and crossreactivity of one antibody with a muscle protein, J. Histochem. Cytochem. 1989, 37, 159-164. [Pg.487]

Labbe, J.R, Mornet, D., Roseau, G., and Kassab, R. (1982) Cross-linking of F-actin to skeletal muscle myosin subfragment 1 with bis(imido esters) Further evidence for the interaction of myosin-head heavy chain with an actin dimer. Biochemistry 21, 6897-6902. [Pg.1085]

Tyrosine phosphorylation plays an important role in synaptic transmission and plasticity. Evidence for this role is that modulators of PTKs and PTPs have been shown to be intimately involved in these synaptic functions. Among the various modulators of PTKs, neuro-trophins have been extensively studied in this regard and will be our focus in the following discussion (for details of growth factors, see Ch. 27). BDNF and NT-3 have been shown to potentiate both the spontaneous miniature synaptic response and evoked synaptic transmission in Xenopus nerve-muscle cocultures. Neurotrophins have also been reported to augment excitatory synaptic transmission in central synapses. These effects of neurotrophins in the neuromuscular and central synapses are dependent on tyrosine kinase activities since they are inhibited by a tyrosine kinase inhibitor, K-252a. Many effects of neurotrophins on synaptic functions have been attributed to the enhancement of neurotransmitter release BDNF-induced increase in neurotransmitter release is a result of induced elevation in presynaptic cytosolic calcium. Accordingly, a presynaptic calcium-depen-dent phenomenon - paired pulse facilitation - is impaired in mice deficient in BDNF. [Pg.430]

Nickel retention in the body of mammals is low. The half-time residence of soluble forms of nickel is several days, with little evidence for tissue accumulation except in the lung (USEPA 1980, 1986). Radionickel-63 (63Ni) injected into rats and rabbits cleared rapidly most (75%) of the injected dose was excreted within 24 to 72 h (USEPA 1980). Nickel clears at different rates from various tissues. In mammals, clearance was fastest from serum, followed by kidney, muscle, stomach, and uterus relatively slow clearance was evident in skin, brain, and especially lung (Kasprzak 1987). The half-time persistence in human lung for insoluble forms of nickel is 330 days (Sevin 1980). [Pg.451]

There is no evidence to support the efficacy of muscle relaxants for tension-type headache. [Pg.625]

Blaustein We have seen the same thing in cultured cells we see no evidence for CICR. There are two possible explanations. First, the smooth muscle cells have a different ryanodine receptor isoform. Second, the rate of rise of Ca2+ is much slower in smooth muscle. In cardiac muscle there is a blast of Ca2+, with a rapid rise. Perhaps the slower effect means that smooth muscle cells don t get to threshold at the ryanodine receptor. The question is whether it is the channel or the process in general. [Pg.24]

Fry The voltage dependence of these STOCs that you have shown is interesting, because there is now more evidence for T type Ca2+ currents in smooth muscle cells. Kenton Sanders, you said that it was in the window current for the L-type Ca2+ channels, but it is probably about 10 mV too negative for that. Is there any evidence that T type channel activity will be involved ... [Pg.67]

Blaustein Here you have really good evidence for some kind of Ca2+ induced release and the role of RyRs in activation of the muscle. This is very different from the kinds of things that Mark Nelson has shown in vascular smooth muscle, where release of Ca2+ from RyRs is involved in relaxation. Isn t this a good example of the enormous diversity in different tissues. Smooth muscle is so diverse when compared with cardiac or skeletal muscle. [Pg.122]

Parekh AB, Penner R 1997 Store depletion and calcium influx. Physiol Rev 77 901-930 Potocnik SJ, Hill MA 2001 Pharmacological evidence for capacitative Ca2+ entry in cannulated and pressurized skeletal muscle arterioles. Br J Pharmacol 134 247-256 Pozzan T, Rizzuto R, Volpe P, Meldolesi J 1994 Molecular and cellular physiology of intracellular calcium stores. Physiol Rev 74 595—636 Putney JW Jr, Broad LM, Braun FJ, Lievremont JP, Bird GS 2001 Mechanisms of capacitative calcium entry. J Cell Sci 114 2223—2229... [Pg.137]

Work on vascular smooth muscle has not led to any real consensus as to the precise differences in SR function between normal and hypertensive animals, although there is evidence, summarized in a review by Raeymaekers Wuytack (1993) for diminished SR Ca2+ transport in hypertensive animals. More recent work has also provided evidence for increased Ca2+ influx from the extracellular space in vascular smooth muscles from various rat models of hypertension (Nomura et al 1997, Arii et al 1999). [Pg.246]

Kotlikoff I have a question about InsP3 receptors and ryanodine receptors. There is good evidence for wave propagation with both systems in smooth muscle. Can you say anything in experiments where you have looked with antibodies about the relationship between InsP3 receptors and ryanodine receptors And does this provide any insight into the interaction between these Ca2+-sensitive intracellular Ca2+ release channels ... [Pg.269]


See other pages where Muscle evidence for is mentioned: [Pg.191]    [Pg.863]    [Pg.1036]    [Pg.1276]    [Pg.168]    [Pg.212]    [Pg.229]    [Pg.405]    [Pg.247]    [Pg.110]    [Pg.16]    [Pg.266]    [Pg.325]    [Pg.180]    [Pg.169]    [Pg.74]    [Pg.185]    [Pg.85]    [Pg.99]    [Pg.427]    [Pg.59]    [Pg.905]    [Pg.181]    [Pg.308]    [Pg.372]    [Pg.723]    [Pg.236]    [Pg.236]   
See also in sourсe #XX -- [ Pg.632 ]




SEARCH



Evidence for

Evidence for Translocation of Enzymes during Smooth Muscle Activation

© 2024 chempedia.info