LINC complexes in health and disease

被引：153

作者：

Mejat, Alexandre ^{[1
]}

Misteli, Tom ^{[1
]}

机构：

[1] NCI, NIH, Bethesda, MD 20892 USA

来源：

NUCLEUS | 2010年 / 1卷 / 01期

关键词：

LINC; lamins A/C; LMNA; SUN; nesprins; EDMD;

D O I：

10.4161/nucl.1.1.10530

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

The cell nucleus communicates with the rest of the cell via nucleo/cytoplasmic transport of proteins and RNA through the nuclear pores. Direct mechanical links between the nucleus and the cytoplasm have recently emerged in the form of LINC (Linkers of the nucleoskeleton to the cytoskeleton) protein complexes. A LINC complex consists of four components. At its core are an inner nuclear membrane (INM) transmembrane protein and an outer nuclear membrane (ONM) transmembrane protein which physically interact with each other in the lumen of the NE. The INM LINC component interacts on the nucleoplasmic side with either the lamina or with an INM-associated protein. The ONM LINC component on the other hand contacts on the cytoplasmatic side a component of the cytoskeleton. This review highlights the components of LINC complexes and their emerging roles in mechanotransduction, nuclear migration, chromosome positioning, signaling, meiosis, cytoskeletal organization and human disease.

引用

页码：40 / 52

页数：13

共 141 条

[1]

Lack of desmin results in abortive muscle regeneration and modifications in synaptic structure [J].

Agbulut, O ;

Li, ZL ;

Périé, S ;

Ludosky, MA ;

Paulin, D ;

Cartaud, J ;

Butler-Browne, G .

CELL MOTILITY AND THE CYTOSKELETON, 2001, 49 (02) :51-66

[2]

Syne-1, a dystrophin- and klarsicht-related protein associated with synaptic nuclei at the neuromuscular junction [J].

Apel, ED ;

Lewis, RM ;

Grady, RM ;

Sanes, JR .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (41) :31986-31995

[3]

Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies [J].

Arimura, T ;

Helbling-Leclerc, A ;

Varnous, S ;

Niel, F ;

Lacène, E ;

Fromes, Y ;

Toussaint, M ;

Mura, AM ;

Keller, DI ;

Amthor, H ;

Isnard, R ;

Malissen, M ;

Schwartz, K ;

Bonne, G .

HUMAN MOLECULAR GENETICS, 2005, 14 (01) :155-169

[4]

Attali R, 2009, HUM MOL GENET

[5]

The Supramolecular Organization of the C. elegans Nuclear Lamin Filament [J].

Ben-Harush, Kfir ;

Wiesel, Naama ;

Frenkiel-Krispin, Daphna ;

Moeller, Dorothee ;

Soreq, Eyal ;

Aebi, Ueli ;

Herrmann, Harald ;

Gruenbaum, Yosef ;

Medalia, Ohad .

JOURNAL OF MOLECULAR BIOLOGY, 2009, 386 (05) :1392-1402

[6]

THE GENE FOR A NOVEL HUMAN LAMIN MAPS AT A HIGHLY TRANSCRIBED LOCUS OF CHROMOSOME-19 WHICH REPLICATES AT THE ONSET OF S-PHASE [J].

BIAMONTI, G ;

GIACCA, M ;

PERINI, G ;

CONTREAS, G ;

ZENTILIN, L ;

WEIGHARDT, F ;

GUERRA, M ;

DELLAVALLE, G ;

SACCONE, S ;

RIVA, S ;

FALASCHI, A .

MOLECULAR AND CELLULAR BIOLOGY, 1992, 12 (08) :3499-3506

[7]

BIONE S, 1995, HUM MOL GENET, V4, P1859

[8]

IDENTIFICATION OF A NOVEL X-LINKED GENE RESPONSIBLE FOR EMERY-DREIFUSS MUSCULAR-DYSTROPHY [J].

BIONE, S ;

MAESTRINI, E ;

RIVELLA, S ;

MANCINI, M ;

REGIS, S ;

ROMEO, G ;

TONIOLO, D .

NATURE GENETICS, 1994, 8 (04) :323-327

[9]

Bonne G, 2003, LANCET, V362, P1585, DOI 10.1016/S0140-6736(03)14761-7

[10]

Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy [J].

Bonne, G ;

Di Barletta, MR ;

Varnous, S ;

Bécane, HM ;

Hammouda, EH ;

Merlini, L ;

Muntoni, F ;

Greenberg, CR ;

Gary, F ;

Urtizberea, JA ;

Duboc, D ;

Fardeau, M ;

Toniolo, D ;

Schwartz, K .

NATURE GENETICS, 1999, 21 (03) :285-288

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