Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation
By T. McKinsey, Chun-li Zhang, Jian-rong Lu, E. Olson. Nature, 2000
1,105 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/e526f22a4af11a78c39c1ae6c924e22714fad85a
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In Molecular Biology
- E. Olson
- C. Bentzinger
- Nicolas A. Dumont
- Marie-Claude Sincennes
- E. Nestler
- V. Krishnan
- R. Bassel-Duby
- J. Richardson
Citations in the corpus
- Histone deacetylase 4 controls chondrocyte hypertrophy during skeletogenesis. (2004, background): “…A chondrocyte-specific HDAC4 transgene was constructed by sub-Cartilage and Bone Staining cloning the signal-resistant HDAC4-S/A mutant, in which serinesEmbryonic or newborn mice were skinned, eviscerated, and fixed 246, 467, and 632 were changed to alanines (McKinsey et al., 2000b),in ethanol.”
- HDAC family: What are the cancer relevant targets? (2009, background): “Hdac7 is specifically expressed in the vascular endothelium during early embryogenesis, where it maintains vascular integrity by repressing the expression of matrix metalloproteinase 10 by associating with myocyte enhancer factor-2 (MEF2) [32].”
- The SMRT and N-CoR Corepressors Are Activating Cofactors for Histone Deacetylase 3 (2001, background): “Gal4SMRT DAD mutants W432A, F440A, F451A, I454A, L458A, V463A, and Y470A were produced using the corresponding mutagenic oligonucleotides and the QuickChange site-directed mutagenesis kit (Stratagene).”
- Histone deacetylase 5 epigenetically controls behavioral adaptations to chronic emotional stimuli. (2007, positive): “Studies in nonneural cells suggest that phosphorylation of Ser259 (along with a cooperatively regulated site at Ser498) provides docking sites for 14-3-3 proteins, which mediate the export of HDAC5 out of the nucleus (McKinsey et al., 2000a, 2000b).”
- Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility. (2007, background): “Class II HDACs regulate tissue growth through signal-dependent repression of MEF2 and other transcription factors (McKinsey et al. 2000).”
- Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development (2004, background): “Neither cyclic AMP nor activated protein kinase A promotes the phosphorylation or nuclear export of class II HDACs (27).”
- microRNA-1 and microRNA-206 regulate skeletal muscle satellite cell proliferation and differentiation by repressing Pax7 (2010, background): “HDAC4 was also shown repressed by miR-206 (Lu et al., 2000; McKinsey et al., 2000; Chen et al., 2006; Williams et al., 2009).”
- Fiber types in mammalian skeletal muscles. (2011, background): “In cultured muscle cells, the activity of MEF2 is controlled by class II histone deacetylases (HDACs), HDAC4 and HDAC5, that bind to MEF2 and repress MEF2-dependent genes: MEF2 activity is induced by HDAC kinases, such as calcium- and calmodulin-dependent protein kinase (CaMK), that cause phosphoryl”