The many roles of histone deacetylases in development and physiology: implications for disease and therapy
By M. Haberland, Rusty L. Montgomery, E. Olson. Nature reviews genetics, 2009
2,507 citations recorded by the source corpus.
Histone deacetylases (HDACs) are part of a vast family of enzymes that have crucial roles in numerous biological processes, largely through their repressive influence on transcription. The expression of many HDAC isoforms in eukaryotic cells raises questions about their possible specificity or redundancy, and whether they control global or specific programmes of gene expression. Recent analyses of HDAC knockout mice have revealed highly specific functions of individual HDACs in development and disease. Mutant mice lacking individual HDACs are a powerful tool for defining the functions of HDACs in vivo and the molecular targets of HDAC inhibitors in disease.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/cda2d97fd93be48511d0cda64f8ba9d27c7f5877
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Citations in the corpus
- The Short Chain Fatty Acid Butyrate Imprints an Antimicrobial Program in Macrophages (2019, background): “We initially treated macrophages with TMP195, an inhibitor of HDAC class IIa (Davie, 2003) that has been used to activate tumor-associated macrophages (Guerriero et al., 2017) and with tubacin that targets HDAC class IIb.”
- Erasers of histone acetylation: the histone deacetylase enzymes. (2014, background): “There is much evidence to support the fact that heart diseases are linked to abnormal HDAC expression or activity (reviewed by Haberland et al. 2009).”
- Influence of Metabolism on Epigenetics and Disease (2013, neutral): “These enzymes come in two flavors, those that catalyze deacetylation in an NAD+-independent manner, yielding the deacetylated substrate and free acetate as products; and those that are NAD+-dependent, yielding O-acetyl-ADP-ribose, the deacetylated substrate, and nicotinamide as products (Denu, 2005;”
- Histone Deacetylase Inhibitors as Anticancer Drugs (2017, background): “prenatally with severe proliferation defects and general growth retardation; HDAC2-null mice die the first day after birth for cardiac malformations; and HDAC3-null mice die prenatally for defects in gastrulation [3,4].”
- Kidney fibrosis: from mechanisms to therapeutic medicines (2023, background): “Sirtuin (SIRT) 1–7 are the members of III HDACs, and HDAC11 is only one of IV HDAC.(187) The pan HDAC I and II inhibitor Trichostatin A could delay fibrotic kidney via suppressing TGF-β1 and JNK/Notch2 pathways,(190,199) as well as preserving E-cadherin expression.”
- Epigenetics: A Molecular Link Between Environmental Factors and Type 2 Diabetes (2009, background): “, HDAC inhibitors, can be used in the treatment of diabetic complications (13,111,112).”
- Virtual Ligand Screening of the p300/CBP Histone Acetyltransferase: Identification of a Selective Small Molecule Inhibitor (2010, background): “Acetylation on protein lysine residues is catalyzed by histone acetyltransferases (HATs) and acetyl-Lys cleavage is performed by histone deacetylases (HDACs) (Hodawadekar and Marmorstein, 2007; Haberland et al., 2009; Cole, 2008).”
- The outs and the ins of sphingosine-1-phosphate in immunity (2011, neutral): “Histone deacetylases (HDACs) remove acetyl groups from histones, thereby inducing chromatin condensation and transcriptional repression, and have emerged as key targets to reverse aberrant epigenetic changes associated with human diseases, such as cancer and inflammatio”