Loss of nucleoplasmic LAP2α–lamin A complexes causes erythroid and epidermal progenitor hyperproliferation-Reference-Cited by-同舟云学术

Loss of nucleoplasmic LAP2α–lamin A complexes causes erythroid and epidermal progenitor hyperproliferation

Published:2008-10-12 Issue:11 Volume:10 Page:1341-1348
ISSN:1465-7392
Container-title:Nature Cell Biology
language:en
Short-container-title:Nat Cell Biol

Author:

Naetar Nana,Korbei Barbara,Kozlov Serguei,Kerenyi Marc A.,Dorner Daniela,Kral Rosana,Gotic Ivana,Fuchs Peter,Cohen Tatiana V.,Bittner Reginald,Stewart Colin L.,Foisner Roland

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology

Link

http://www.nature.com/articles/ncb1793.pdf

Reference33 articles.

1. Dechat, T. et al. Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin. Genes Dev. 22, 832–853 (2008).

2. Schirmer, E. C. & Foisner, R. Proteins that associate with lamins: many faces, many functions. Exp. Cell Res. 313, 2167–2179 (2007).

3. Capell, B. C. & Collins, F. S. Human laminopathies: nuclei gone genetically awry. Nature Rev. Genet. 7, 940–952 (2006).

4. Dorner, D. et al. Lamina-associated polypeptide 2α regulates cell cycle progression and differentiation via the retinoblastoma–E2F pathway. J. Cell Biol. 173, 83–93 (2006).

5. Pekovic, V. et al. Nucleoplasmic LAP2α–lamin A complexes are required to maintain a proliferative state in human fibroblasts. J. Cell Biol. 176, 163–172 (2007).

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