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注意：仅列出部分参考文献，下载原文获取全部文献信息。Mutations of Tropomyosin 3 (TPM3) are Common and Associated With Type 1 Myofiber Hypotrophy in Congenital Fiber Type Disproportion
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Thin filament length dysregulation contributes to muscle weakness in nemaline myopathy patients with nebulin deficiency
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Nebulin Alters Cross-bridge Cycling Kinetics and Increases Thin Filament Activation A NOVEL MECHANISM FOR INCREASING TENSION AND REDUCING TENSION COST
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Length-tension relationship of the external anal sphincter muscle: implications for the anal canal function
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Mutations in TPM3 are a common cause of congenital fiber type disproportion
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Identification of a founder mutation in TPM3 in nemaline myopathy patients of Turkish origin
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EUROPEAN JOURNAL OF HUMAN GENETICS (2008)
Defective regulation of contractile function in muscle fibres carrying an E41K β-tropomyosin mutation
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Skeletal muscle fatigue: Cellular mechanisms
D. G. Allen et al.
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Nemaline myopathy with minicores caused by mutation of the CFL2 gene encoding the skeletal muscle actin-binding protein, cofilin-2
Pankaj B. Agrawal et al.
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Nebulin regulates thin filament length, contractility, and Z-disk structure in vivo
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EMBO JOURNAL (2006)
Nebulin-deficient mice exhibit shorter thin filament lengths and reduced contractile function in skeletal muscle
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When contractile proteins go bad: the sarcomere and skeletal muscle disease
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An alpha-Tropomyosin mutation alters dimer preference in nemaline myopathy
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Clinical course correlates poorly with muscle pathology in nemaline myopathy
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Skeletal muscle of mice with a mutation in slow α-tropomyosin is weaker at lower lengths
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Mutations of the slow muscle α-tropomyosin gene, TPM3, are a rare cause of nemaline myopathy
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Clinical and genetic heterogeneity in nemaline myopathy - a disease of skeletal muscle thin filaments
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Alteration of tropomyosin function and folding by a nemaline myopathy-causing mutation
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