Muscle atrophy in Titin M-line deficient mice (Q58178411)

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K. Raddatz

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S. Labeit

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H. Granzier

Journal of Muscle Research & Cell Motility

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publication date

10 February 2006

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published in

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volume

26

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issue

6-8

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page(s)

381-388

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cites work

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Mutations of TTN, encoding the giant muscle filament titin, cause familial dilated cardiomyopathy

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Extracellular signal-regulated kinase 2 interacts with and is negatively regulated by the LIM-only protein FHL2 in cardiomyocytes

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Identification of muscle specific ring finger proteins as potential regulators of the titin kinase domain

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The molecular composition of the sarcomeric M-band correlates with muscle fiber type

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Cardiomyopathy in zebrafish due to mutation in an alternatively spliced exon of titin

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Fiber type-specific distribution of M-band proteins in chicken muscle

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Molecular structure of the sarcomeric Z-disk: two types of titin interactions lead to an asymmetrical sorting of alpha-actinin.

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Subcellular targeting of metabolic enzymes to titin in heart muscle may be mediated by DRAL/FHL-2

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The NH2 terminus of titin spans the Z-disc: its interaction with a novel 19-kD ligand (T-cap) is required for sarcomeric integrity

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Induction of MafBx and Murf ubiquitin ligase mRNAs in rat skeletal muscle after LPS injection

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A calcineurin-dependent transcriptional pathway controls skeletal muscle fiber type

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Vertical agarose gel electrophoresis and electroblotting of high-molecular-weight proteins

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Titins: giant proteins in charge of muscle ultrastructure and elasticity

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A targeted deletion of the C-terminal end of titin, including the titin kinase domain, impairs myofibrillogenesis.

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The muscular dystrophy with myositis (mdm) mouse mutation disrupts a skeletal muscle-specific domain of titin

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Both synchronous and asynchronous muscle isoforms of projectin (the Drosophila bent locus product) contain functional kinase domains

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Extensibility of isoforms of cardiac titin: variation in contour length of molecular subsegments provides a basis for cellular passive stiffness diversity

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A functional knock-out of titin results in defective myofibril assembly.

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Reeler/Disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2

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