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Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
High mobility group 1 (HMGB1) protein is both a nuclear factor and a secreted protein. In the cell nucleus it acts as an architectural chromatin-binding factor that bends DNA and promotes proteinExpand
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Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
This corrects the article DOI: 10.1038/nature00858
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High mobility of proteins in the mammalian cell nucleus
The mammalian cell nucleus contains numerous sub-compartments, which have been implicated in essential processes such as transcription and splicing. The mechanisms by which nuclear compartments areExpand
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Lamin A-Dependent Nuclear Defects in Human Aging
Mutations in the nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HGPS). Whether lamin A plays any role in normal aging is unknown. We show that theExpand
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Hyperdynamic plasticity of chromatin proteins in pluripotent embryonic stem cells.
Differentiation of embryonic stem (ES) cells from a pluripotent to a committed state involves global changes in genome expression patterns. Gene activity is critically determined by chromatinExpand
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Regulation of Alternative Splicing by Histone Modifications
Histones and Alternative Splicing Alternative splicing—the inclusion of different combinations of gene exons within a messenger RNA transcript—occurs in the majority of human genes and is regulatedExpand
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Ubiquitination Regulates PTEN Nuclear Import and Tumor Suppression
The PTEN tumor suppressor is frequently affected in cancer cells, and inherited PTEN mutation causes cancer-susceptibility conditions such as Cowden syndrome. PTEN acts as a plasma-membraneExpand
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Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome
Hutchinson-Gilford progeria syndrome (HGPS) is a childhood premature aging disease caused by a spontaneous point mutation in lamin A (encoded by LMNA), one of the major architectural elements of theExpand
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RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)
Activated RAS promotes dimerization of members of the RAF kinase family. ATP-competitive RAF inhibitors activate ERK signalling by transactivating RAF dimers. In melanomas with mutant BRAF(V600E),Expand
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Beyond the Sequence: Cellular Organization of Genome Function
Genomes are more than linear sequences. In vivo they exist as elaborate physical structures, and their functional properties are strongly determined by their cellular organization. I discuss here theExpand
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