PMID- 27974395
OWN - NLM
STAT- MEDLINE
DCOM- 20170706
LR  - 20181025
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 131
IP  - 2
DP  - 2017 Jan 1
TI  - Lamins and metabolism.
PG  - 105-111
AB  - 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 familial 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-Gilford 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.
CI  - (c) 2016 The Author(s). published by Portland Press Limited on behalf of the 
      Biochemical Society.
FAU - Charar, Chayki
AU  - Charar C
AD  - Department of Genetics, The Alexander Silberman Institute of Life Sciences, 
      Hebrew University of Jerusalem, Jerusalem 91904, Israel chayki18@gmail.com 
      gru@vms.huji.ac.il.
FAU - Gruenbaum, Yosef
AU  - Gruenbaum Y
AD  - Department of Genetics, The Alexander Silberman Institute of Life Sciences, 
      Hebrew University of Jerusalem, Jerusalem 91904, Israel chayki18@gmail.com 
      gru@vms.huji.ac.il.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Lamins)
SB  - IM
MH  - Aging/genetics/*metabolism
MH  - Animals
MH  - Genetic Diseases, Inborn/genetics/*metabolism
MH  - Humans
MH  - Lamins/genetics/*metabolism
MH  - Metabolic Diseases/genetics/*metabolism
OTO - NOTNLM
OT  - cell cycle
OT  - insulin
OT  - laminopathies
OT  - lamins
OT  - mTOR
OT  - metabolism
OT  - nuclear organization
EDAT- 2016/12/16 06:00
MHDA- 2017/07/07 06:00
CRDT- 2016/12/16 06:00
PHST- 2016/06/30 00:00 [received]
PHST- 2016/10/27 00:00 [revised]
PHST- 2016/11/07 00:00 [accepted]
PHST- 2016/12/16 06:00 [entrez]
PHST- 2016/12/16 06:00 [pubmed]
PHST- 2017/07/07 06:00 [medline]
AID - CS20160488 [pii]
AID - 10.1042/CS20160488 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 2017 Jan 1;131(2):105-111. doi: 10.1042/CS20160488.