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The inner nuclear membrane protein Lem2 is critical for normal nuclear envelope morphology
Author(s) -
Ulbert Sebastian,
Antonin Wolfram,
Platani Melpomeni,
Mattaj Iain W.
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.10.060
Subject(s) - lamin , nuclear lamina , microbiology and biotechnology , inner membrane , chromatin , transmembrane protein , biology , nuclear protein , membrane protein , nuclear membrane , genetics , nucleus , membrane , transcription factor , gene , receptor , mitochondrion
The inner nuclear membrane (INM) of eukaryotic cells is characterized by a unique set of transmembrane proteins which interact with chromatin and/or the nuclear lamina. The number of identified INM proteins is steadily increasing, mainly as a result of proteomic and computational approaches. However, despite a link between mutation of several of these proteins and disease, the function of most transmembrane proteins of the INM remains unknown and depletion of many of these proteins from a variety of systems did not produce an obvious phenotype in the affected cells. Here, we report that depletion of the conserved INM protein Lem2 from human cell lines leads to abnormally shaped nuclei and severely reduces cell survival. We suggest that interactions of Lem2 with lamins or chromatin are critical for maintaining the integrity of the nuclear envelope.