Transcriptional repression, apoptosis, human disease and the functional evolution of the nuclear lamina

Merav Cohen, Yosef Gruenbaum, Kenneth K. Lee, Katherine L. Wilson

Research output: Contribution to journalReview articlepeer-review

205 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)41-47
Number of pages7
JournalTrends in biochemical sciences
Volume26
Issue number1
DOIs
StatePublished - Jan 1 2001

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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