{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T01:34:08Z","timestamp":1791423248368,"version":"4.3.3"},"reference-count":64,"publisher":"Portland Press Ltd.","issue":"2","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,1,1]]},"abstract":"<jats:p>Lamins are nuclear intermediate filaments (IFs) with important roles in most nuclear activities, including nuclear organization and cell-cycle progression. Mutations in human lamins cause over 17 different diseases, termed laminopathies. Most of these diseases are autosomal dominant and can be roughly divided into four major groups: muscle diseases, peripheral neuronal diseases, accelerated aging disorders and metabolic diseases including Dunnigan type\u00a0familial partial lipodystrophy (FLPD), acquired partial lipodystrophy (APL) and autosomal dominant leucodystrophy. Mutations in lamins are also associated with the metabolic syndrome (MS). Cells derived from patients suffering from metabolic laminopathies, as well as cells derived from the corresponding animal models, show a disruption of the mechanistic target of rapamycin (mTOR) pathway, abnormal autophagy, altered proliferative rate and down-regulation of genes that regulate adipogenesis. In addition, treating Hutchinson\u2013Gilford progeria syndrome (HGPS) cells with the mTOR inhibitor rapamycin improves their fate. In this review, we will discuss the ways by which lamin genes are involved in the regulation of cell metabolism.<\/jats:p>","DOI":"10.1042\/cs20160488","type":"journal-article","created":{"date-parts":[[2016,12,15]],"date-time":"2016-12-15T01:40:21Z","timestamp":1481766021000},"page":"105-111","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Lamins and metabolism"],"prefix":"10.1042","volume":"131","author":[{"given":"Chayki","family":"Charar","sequence":"first","affiliation":[{"name":"Department of Genetics, The Alexander Silberman Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem 91904, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yosef","family":"Gruenbaum","sequence":"additional","affiliation":[{"name":"Department of Genetics, The Alexander Silberman Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem 91904, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2016,12,14]]},"reference":[{"key":"2021113010515458500_B1","doi-asserted-by":"publisher","first-page":"137","DOI":"10.1242\/jcs.1984.Supplement_1.10","article-title":"Organization and modulation of nuclear lamina structure","volume":"1","author":"Gerace","year":"1984","journal-title":"J. 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