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- W7934679 abstract "Audrey J. Caudron1, Agnieszka M. Lichanska2, Helen M. Cooper3 and Peter G. Noakes1. 1School of Biomedical Sciences, University of Queensland, Brisbane, Australia. 2 Institute of Molecular Biosciences, University of Queensland, Brisbane, Australia. 3Queensland Brain Institute, University of Queensland, Brisbane, Australia Differential expression of mRNA in MuSK-deficient mice Agrin, a motor nerve derived signal, binds to its receptor the Muscle Specific Kinase (MuSK) to induce the clustering of acetylcholine receptors (AChRs) and other postsynaptic molecules during the formation of the neuromuscular junction (NMJ). MuSK-/- mutant mice display an absence of AChR clusters and an increase in motoneuron survival and muscle nerve branching. These profound defects in both pre- and post-synaptic specialisations suggest that MuSK is a key molecule involved in the inductive interactions between growing motor axons and differentiating muscle cells, essential for healthy synapse formation. We have generated diaphragm muscle mRNA expression profiles from MuSK-deficient E15 embryos and their respective littermate wild-type controls, using Affymetrix® microarrays. Of 20 candidate genes found to be up or down regulated in MuSK-deficient muscles compared to wild-type muscles, 3 have been confirmed to be differentially expressed in MuSK mutants by real-time PCR (Quantitative PCR). Zyxin, a cell adhesion molecule, Mlf-1, a cell cycle regulator and the alpha-AChR (in diaphragm and limb muscles). Our results suggest that these genes are regulated by the neural Agrin-MuSK pathway and could explain the phenotypic differences seen between the wild-type and the mutant mice." @default.
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- W7934679 date "2005-01-01" @default.
- W7934679 modified "2023-09-24" @default.
- W7934679 title "Differential Expression of MRNA in MuSK-Deficient Mice" @default.
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