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

A molecular defect in virally transformed muscle cells that cannot cluster acetylcholine receptors.

Muscle cells infected at the permissive temperature with temperature-sensitive mutants of Rous sarcoma virus and shifted to the non-permissive temperature form myotubes that are unable to cluster acetylcholine receptors (Anthony, D. T., S. M. Schuetze, and L. L. Rubin. 1984. Proc. Natl. Acad. Sci. USA. 81:2265-2269). Work described in this paper demonstrates that the virally-infected cells are missing a 37-kD peptide which reacts with an anti-tropomyosin antiserum. Using a monoclonal antibody specific for the missing peptide, we show that this tropomyosin is absent from fibroblasts and is distinct from smooth muscle tropomyosins. It is also different from the two previously identified striated muscle myofibrillar tropomyosins (alpha and beta). We suggest that, in normal muscle, this novel, non-myofibrillar, tropomyosin-like molecule is an important component of a cytoskeletal network necessary for cluster formation.[1]


  1. A molecular defect in virally transformed muscle cells that cannot cluster acetylcholine receptors. Anthony, D.T., Jacobs-Cohen, R.J., Marazzi, G., Rubin, L.L. J. Cell Biol. (1988) [Pubmed]
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