Abstract
The striated muscle specific Lin 12, Islet 1, Mec 3 (LIM)-only protein MLP is a conserved positive regulator of myogenic differentiation associated with the actin-based cytoskeleton and the cell nucleus [1,2]. In the heart, MLP is expressed at high levels in atrial and ventricular myocytes during development and in the adult [1]. MLP consists of two LIM double-zinc fingers linked by a spacer of 58 residues. The LIM motif is a protein binding interface found in a diverse group of proteins [3]. MLP may promote myogenic differentiation by both acting as a molecular adapter to modulate protein assembly along the actin-based cytoskeleton, and by promoting muscle specific gene expression as a transcriptional co-factor. This hypothesis is supported by the demonstration that the second LIM motif of MLP can specifically target interacting proteins to the actin-based cytoskeleton [2], and the first LIM motif mediates the interaction of MLP with muscle-specific transcription factors [4].
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© 1999 Springer Science+Business Media Dordrecht
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Caroni, P. (1999). Mice Deficient in Muscle LIM Protein (MLP) Reveal a Pathway to Dilated Cardiomyopathy and Heart Failure. In: Doevendans, P.A., Reneman, R.S., van Bilsen, M. (eds) Cardiovascular Specific Gene Expression. Developments in Cardiovascular Medicine, vol 214. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9321-2_4
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DOI: https://doi.org/10.1007/978-94-015-9321-2_4
Publisher Name: Springer, Dordrecht
Print ISBN: 978-90-481-5189-9
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