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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review


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Disease relevance of Sarcolemma


Psychiatry related information on Sarcolemma

  • This protein is absent in DMD cases, wherefore, the sarcolemma undergoes a segmentary necrosis losing its contractile property during eccentric and concentric physical activity [6].

High impact information on Sarcolemma


Chemical compound and disease context of Sarcolemma


Biological context of Sarcolemma

  • The impermeant dye antipyrylazo III was used to measure depletion of extracellular calcium and net influx of calcium through the sarcolemma during the cardiac action potential [17].
  • However, agonist competition studies with both carbachol and oxotremorine showed that it was a loss of high affinity agonist binding sites in the sarcolemma from failing LV that accounted for this difference [18].
  • Since muscle GLUT4 glucose transporter levels are normal in type 2 diabetes, we have tested the hypothesis that insulin resistance is due to impaired translocation of intracellular GLUT4 to sarcolemma [19].
  • These findings strongly support the proposition that the primary function of dystrophin is to provide mechanical reinforcement to the sarcolemma and thereby protect it from the membrane stresses developed during muscle contraction [20].
  • To illustrate their use in dystrophin analysis, a Duchenne patient with a frameshift deletion of exons 42 and 43 makes a truncated dystrophin encoded by exons 1-41, and we now show that this can be detected in the sarcolemma by mAbs up to and including those specific for exon 41 epitopes but not by mAbs specific for exon 43 or later epitopes [21].

Anatomical context of Sarcolemma


Associations of Sarcolemma with chemical compounds

  • We conclude that dystrophin is linked to an integral membrane glycoprotein in the sarcolemma [23].
  • In these experiments, up to 79% of the total tissue sialic acid was removed, and electron microscopy studies showed that this removal was accompanied by marked reduction of lanthanum binding to the sarcolemma [27].
  • The striking absence of an inotropic action by isoproterenol on atria in sodium-free media suggests that sodium (and possibly a sodium-calcium exchange across the sarcolemma) plays an important role in the inotropic action of catecholamines [28].
  • Even at 100-fold greater concentrations of methacholine, significantly less inhibition of adenylate cyclase activity was observed in LV failure as compared with normal LV sarcolemma [18].
  • The GLUT4 increments in the 32% sucrose fraction were correlated with maximal in vivo glucose disposal rates (r = +0.51, P = 0.026), and, therefore, represented GLUT4 recruitment to sarcolemma or a quantitative marker for this process [19].

Gene context of Sarcolemma


Analytical, diagnostic and therapeutic context of Sarcolemma


  1. Duchenne muscular dystrophy: deficiency of dystrophin at the muscle cell surface. Bonilla, E., Samitt, C.E., Miranda, A.F., Hays, A.P., Salviati, G., DiMauro, S., Kunkel, L.M., Hoffman, E.P., Rowland, L.P. Cell (1988) [Pubmed]
  2. Immunohistochemical analysis of dystrophin-associated proteins in Becker/Duchenne muscular dystrophy with huge in-frame deletions in the NH2-terminal and rod domains of dystrophin. Matsumura, K., Burghes, A.H., Mora, M., Tomé, F.M., Morandi, L., Cornello, F., Leturcq, F., Jeanpierre, M., Kaplan, J.C., Reinert, P. J. Clin. Invest. (1994) [Pubmed]
  3. Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation. Corr, P.B., Creer, M.H., Yamada, K.A., Saffitz, J.E., Sobel, B.E. J. Clin. Invest. (1989) [Pubmed]
  4. Additive effects of hyperinsulinemia and ischemia on myocardial GLUT1 and GLUT4 translocation in vivo. Russell, R.R., Yin, R., Caplan, M.J., Hu, X., Ren, J., Shulman, G.I., Sinusas, A.J., Young, L.H. Circulation (1998) [Pubmed]
  5. Cardiolipin-protein complexes and initiation of complement activation after coronary artery occlusion. Rossen, R.D., Michael, L.H., Hawkins, H.K., Youker, K., Dreyer, W.J., Baughn, R.E., Entman, M.L. Circ. Res. (1994) [Pubmed]
  6. Progressive muscular dystrophy--Duchenne type. Controversies of the kinesitherapy treatment. de Araujo Leitão, A.V., Duro, L.A., de Andrade Penque, G.M. São Paulo medical journal = Revista paulista de medicina. (1995) [Pubmed]
  7. Function and genetics of dystrophin and dystrophin-related proteins in muscle. Blake, D.J., Weir, A., Newey, S.E., Davies, K.E. Physiol. Rev. (2002) [Pubmed]
  8. Carbon dioxide transport and carbonic anhydrase in blood and muscle. Geers, C., Gros, G. Physiol. Rev. (2000) [Pubmed]
  9. Nitric oxide synthase complexed with dystrophin and absent from skeletal muscle sarcolemma in Duchenne muscular dystrophy. Brenman, J.E., Chao, D.S., Xia, H., Aldape, K., Bredt, D.S. Cell (1995) [Pubmed]
  10. Dp71 can restore the dystrophin-associated glycoprotein complex in muscle but fails to prevent dystrophy. Cox, G.A., Sunada, Y., Campbell, K.P., Chamberlain, J.S. Nat. Genet. (1994) [Pubmed]
  11. Defective membrane repair in dysferlin-deficient muscular dystrophy. Bansal, D., Miyake, K., Vogel, S.S., Groh, S., Chen, C.C., Williamson, R., McNeil, P.L., Campbell, K.P. Nature (2003) [Pubmed]
  12. Propranolol treatment externalizes beta-adrenergic receptors in guinea pig myocardium and prevents further externalization by ischemia. Maisel, A.S., Motulsky, H.J., Insel, P.A. Circ. Res. (1987) [Pubmed]
  13. Activation of Na+/Ca2+ exchange by adenosine in ewe heart sarcolemma is mediated by a pertussis toxin-sensitive G protein. Brechler, V., Pavoine, C., Lotersztajn, S., Garbarz, E., Pecker, F. J. Biol. Chem. (1990) [Pubmed]
  14. Hydrogen peroxide changes in ischemic and reperfused heart. Cytochemistry and biochemical and X-ray microanalysis. Slezak, J., Tribulova, N., Pristacova, J., Uhrik, B., Thomas, T., Khaper, N., Kaul, N., Singal, P.K. Am. J. Pathol. (1995) [Pubmed]
  15. Decreased dihydropyridine receptor number in hypertensive rat vascular muscle cells. Hermsmeyer, K., White, A.C., Triggle, D.J. Hypertension (1995) [Pubmed]
  16. Skeletal-muscle sarcolemma from normal and dystrophic mice. Isolation, characterization and lipid composition. de Kretser, T.A., Livett, B.G. Biochem. J. (1977) [Pubmed]
  17. Optical measurements of extracellular calcium depletion during a single heartbeat. Cleemann, L., Pizarro, G., Morad, M. Science (1984) [Pubmed]
  18. Impaired cardiac muscarinic receptor function in dogs with heart failure. Vatner, D.E., Lee, D.L., Schwarz, K.R., Longabaugh, J.P., Fujii, A.M., Vatner, S.F., Homcy, C.J. J. Clin. Invest. (1988) [Pubmed]
  19. Evidence for defects in the trafficking and translocation of GLUT4 glucose transporters in skeletal muscle as a cause of human insulin resistance. Garvey, W.T., Maianu, L., Zhu, J.H., Brechtel-Hook, G., Wallace, P., Baron, A.D. J. Clin. Invest. (1998) [Pubmed]
  20. Dystrophin protects the sarcolemma from stresses developed during muscle contraction. Petrof, B.J., Shrager, J.B., Stedman, H.H., Kelly, A.M., Sweeney, H.L. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  21. Use of epitope libraries to identify exon-specific monoclonal antibodies for characterization of altered dystrophins in muscular dystrophy. Nguyen, T.M., Morris, G.E. Am. J. Hum. Genet. (1993) [Pubmed]
  22. Primary structure and functional expression of the cardiac dihydropyridine-sensitive calcium channel. Mikami, A., Imoto, K., Tanabe, T., Niidome, T., Mori, Y., Takeshima, H., Narumiya, S., Numa, S. Nature (1989) [Pubmed]
  23. Association of dystrophin and an integral membrane glycoprotein. Campbell, K.P., Kahl, S.D. Nature (1989) [Pubmed]
  24. F-actin binding site masked by the intramolecular association of vinculin head and tail domains. Johnson, R.P., Craig, S.W. Nature (1995) [Pubmed]
  25. Alterations in phospholipid N-methylation of cardiac subcellular membranes due to experimentally induced diabetes in rats. Panagia, V., Taira, Y., Ganguly, P.K., Tung, S., Dhalla, N.S. J. Clin. Invest. (1990) [Pubmed]
  26. Effects of amrinone, a cardiotonic drug, on calcium movements in dog erythrocytes. Parker, J.C., Harper, J.R. J. Clin. Invest. (1980) [Pubmed]
  27. Removal of sialic acid from cardiac sarcolemma does not affect contractile function in electrically stimulated guinea pig left atria. Harding, S.E., Halliday, J. Nature (1980) [Pubmed]
  28. Sodium requirement for the positive inotropic action of isoproterenol on guinea pig atria. Linden, J., Brooker, G. Science (1978) [Pubmed]
  29. The dystrophin complex forms a mechanically strong link between the sarcolemma and costameric actin. Rybakova, I.N., Patel, J.R., Ervasti, J.M. J. Cell Biol. (2000) [Pubmed]
  30. Localization of the DMDL gene-encoded dystrophin-related protein using a panel of nineteen monoclonal antibodies: presence at neuromuscular junctions, in the sarcolemma of dystrophic skeletal muscle, in vascular and other smooth muscles, and in proliferating brain cell lines. Nguyen, T.M., Ellis, J.M., Love, D.R., Davies, K.E., Gatter, K.C., Dickson, G., Morris, G.E. J. Cell Biol. (1991) [Pubmed]
  31. In vivo requirement of the alpha-syntrophin PDZ domain for the sarcolemmal localization of nNOS and aquaporin-4. Adams, M.E., Mueller, H.A., Froehner, S.C. J. Cell Biol. (2001) [Pubmed]
  32. Small, membrane-bound, alternatively spliced forms of ankyrin 1 associated with the sarcoplasmic reticulum of mammalian skeletal muscle. Zhou, D., Birkenmeier, C.S., Williams, M.W., Sharp, J.J., Barker, J.E., Bloch, R.J. J. Cell Biol. (1997) [Pubmed]
  33. Stimulation of calcineurin signaling attenuates the dystrophic pathology in mdx mice. Chakkalakal, J.V., Harrison, M.A., Carbonetto, S., Chin, E., Michel, R.N., Jasmin, B.J. Hum. Mol. Genet. (2004) [Pubmed]
  34. Dystrophin colocalizes with beta-spectrin in distinct subsarcolemmal domains in mammalian skeletal muscle. Porter, G.A., Dmytrenko, G.M., Winkelmann, J.C., Bloch, R.J. J. Cell Biol. (1992) [Pubmed]
  35. A novel mechanism of myocyte degeneration involving the Ca2+-permeable growth factor-regulated channel. Iwata, Y., Katanosaka, Y., Arai, Y., Komamura, K., Miyatake, K., Shigekawa, M. J. Cell Biol. (2003) [Pubmed]
  36. Low-flow ischemia leads to translocation of canine heart GLUT-4 and GLUT-1 glucose transporters to the sarcolemma in vivo. Young, L.H., Renfu, Y., Russell, R., Hu, X., Caplan, M., Ren, J., Shulman, G.I., Sinusas, A.J. Circulation (1997) [Pubmed]
  37. Defects in sarcolemmal Ca2+ transport in hearts due to induction of calcium paradox. Makino, N., Panagia, V., Gupta, M.P., Dhalla, N.S. Circ. Res. (1988) [Pubmed]
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