Transcriptional repression, apoptosis, human disease and the functional evolution of the nuclear lamina.
The number and complexity of genes encoding nuclear lamina proteins has increased during metazoan evolution. Emerging evidence reveals that transcriptional repressors such as the retinoblastoma protein, and apoptotic regulators such as CED-4, have functional and dynamic interactions with the lamina. The discovery that mutations in nuclear lamina proteins cause heritable tissue-specific diseases, including Emery-Dreifuss muscular dystrophy, is prompting a fresh look at the nuclear lamina to devise models that can account for its diverse functions and dynamics, and to understand its enigmatic structure.
Cohen
M
M
Department of Genetics, The Institute of Life Sciences, The Hebrew University of Jerusalem, 91904, Jerusalem, Israel
Lee
K K
KK
Wilson
K L
KL
Gruenbaum
Y
Y
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D022003:Cell Nucleus Structures / Q000235:genetics / Q000378:metabolism; D056890:Eukaryota / Q000502:physiology; D019143:Evolution, Molecular; D005786:Gene Expression Regulation; D030342:Genetic Diseases, Inborn / Q000235:genetics / Q000378:metabolism; D006570:Heterochromatin / Q000378:metabolism; D006801:Humans; D007425:Intracellular Membranes / Q000378:metabolism; D034882:Lamins; D020389:Muscular Dystrophy, Emery-Dreifuss / Q000235:genetics; D009687:Nuclear Proteins / Q000502:physiology*; D014158:Transcription, Genetic
D006570:Heterochromatin; D034882:Lamins; D009687:Nuclear Proteins