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. 2007 Jul 2;8:46. doi: 10.1186/1471-2202-8-46

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Copyright © 2007 Camilleri et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Model for a balance between PTPs such as SHP-2 and kinases such as SFKs, which stabilizes postsynaptic AChR clusters. Process A, stabilization: MuSK-bound and activated SHP-2 could activate SFKs, leading to AChR β phosphorylation, stable AChR-rapsyn (rap) interaction and phosphorylation of cytoskeletal regulators (e.g. actin-controlling proteins such as the SFK-substrates cortactin, p190RhoGAP or WASp). Process B, destabilization: SHP-2 may dephosphorylate AChR β and the cytoskeletal regulators. A balance between A and B keeps clusters intact. UGC, utrophin-glycoprotein complex: an array of proteins that stabilize the postsynaptic apparatus. Members of this complex interact with rapsyn (β-dystroglycan) and actin (utrophin).