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The majority of laminopathies are caused by mutations in the\n                    <jats:italic>LMNA<\/jats:italic>\n                    gene, encoding lamin A\/C, but manifest as diverse pathologies including muscular dystrophy, lipodystrophy, neuropathy, and progeroid syndromes. Lamin\u2010binding proteins implicated in laminopathies include lamin B2, nuclear envelope proteins such as emerin, MAN1, LBR, and nesprins, the nuclear matrix protein matrin 3, the lamina\u2010associated polypeptide, LAP2alpha and the transcriptional regulator FHL1. Thus, the altered functionality of a nuclear proteins network appears to be involved in the onset of laminopathic diseases. The functional interplay among different proteins involved in this network implies signaling partners. The signaling effectors may either modify nuclear envelope proteins and their binding properties, or use nuclear envelope\/lamina proteins as platforms to regulate signal transduction. In this review, both aspects of lamin\u2010linked signaling are presented and the major pathways so far implicated in laminopathies are summarized. J. Cell. Biochem. 112: 979\u2013992, 2011. \u00a9 2010 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jcb.22992","type":"journal-article","created":{"date-parts":[[2010,12,7]],"date-time":"2010-12-07T14:43:25Z","timestamp":1291733005000},"page":"979-992","source":"Crossref","is-referenced-by-count":103,"title":["Laminopathies and lamin\u2010associated signaling pathways"],"prefix":"10.1002","volume":"112","author":[{"given":"Nadir 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