Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR.
By W. Fischle, F. Dequiedt, Michael J Hendzel, M. Guenther, Mitchell A. Lazar, W. Voelter, E. Verdin. Molecules and Cells, 2002
789 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/36bba7b27566d31e7c6f911aff223c2abe947ab2
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In Molecular Biology
- Jessica E. Bolden
- M. Peart
- Jamie E. Hoberg
- Catherine S. Ramsey
- Ricky W. Johnstone
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- A. Kinghorn
In Oncology
Citations in the corpus
- Anticancer activities of histone deacetylase inhibitors (2006, background): “The difficulty of producing recombinant purified HDACs that are functionally active has prevented comprehensive specificity profiling of each HDACi; however, some studies using partially purified and catalytically active recombinant HDACs have been complete”
- IκB Kinase α-Mediated Derepression of SMRT Potentiates Acetylation of RelA/p65 by p300 (2006, background): “However, unlike HDAC1, HDAC3 has the potential to recruit members of the class II HDACs to the repression complex (21).”
- Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “1999), and via the recruitment of class I HDACs and other co-repressors (Fischle et al. 2002; Hohl et al. 2013; Zhang et al. 2002b).”
- A conserved structural motif reveals the essential transcriptional repression function of Spen proteins and their role in developmental signaling. (2003, background): “These corepressors, in turn, repress the level of basal transcription by mediating the assembly of a larger multiprotein complex containing histone deacetylase (HDAC) activity (Heinzel et al. 1997; Nagy et al. 1997; Fischle et al. 2002; Zhang et al. 2002; Yoon et al. 2003).”