Mutations causing Greenberg dysplasia but not Pelger anomaly uncouple enzymatic from structural functions of a nuclear membrane protein-Reference-Cited by-同舟云学术

Mutations causing Greenberg dysplasia but not Pelger anomaly uncouple enzymatic from structural functions of a nuclear membrane protein

Published:2010-07 Issue:4 Volume:1 Page:354-366
ISSN:1949-1034
Container-title:Nucleus
language:en
Short-container-title:Nucleus

Author:

Clayton Peter,Fischer Björn,Mann Anuska,Mansour Sahar,Rossier Eva,Veen Markus,Lang Christine,Baasanjav Sevjidmaa,Kieslich Moritz,Brossuleit Katja,Gravemann Sophia,Schnipper Nele,Karbasyian Mohsen,Demuth Ilja,Zwerger Monika,Vaya Amparo,Utermann Gerd,Mundlos Stefan,Stricker Sigmar,Sperling Karl,Hoffmann Katrin

Publisher

Informa UK Limited

Subject

Cell Biology

Link

http://www.tandfonline.com/doi/pdf/10.4161/nucl.1.4.12435

Reference53 articles.

1. The lamin B receptor of the inner nuclear membrane undergoes mitosis-specific phosphorylation and is a substrate for p34cdc2-type protein kinase.

2. Domain-specific Interactions of Human HP1-type Chromodomain Proteins and Inner Nuclear Membrane Protein LBR

3. Dynamic interactions of nuclear lamina proteins with chromatin and transcriptional machinery

4. Characterization of the human gene encoding LBR, an integral protein of the nuclear envelope inner membrane

5. The Human Lamin B Receptor/Sterol Reductase Multigene Family

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