The histone deacetylase HDAC3 is essential for Purkinje cell function, potentially complicating the use of HDAC inhibitors in SCA1

Disassociation of Histone Deacetylase-3 from Normal Huntingtin Underlies Mutant Huntingtin Neurotoxicity

(2013) F. H. Bardai et al.   JOURNAL OF NEUROSCIENCE

Histone deacetylase-3 interacts with ataxin-7 and is altered in a spinocerebellar ataxia type 7 mouse model

(2013) Carlotta E Duncan et al.   Molecular Neurodegeneration

Histone acetylation: molecular mnemonics on the chromatin

(2013) Johannes Gräff et al.   NATURE REVIEWS NEUROSCIENCE

Histone deacetylase 3 is required for maintenance of bone mass during aging

(2012) Meghan E. McGee-Lawrence et al.   BONE

Selective histone deacetylase (HDAC) inhibition imparts beneficial effects in Huntington's disease mice: implications for the ubiquitin–proteasomal and autophagy systems

(2012) Haiqun Jia et al.   HUMAN MOLECULAR GENETICS

HDAC inhibitor-based therapies: Can we interpret the code?

(2012) Maria New et al.   Molecular Oncology

LANP mediates neuritic pathology in Spinocerebellar ataxia type 1

(2012) Marija Cvetanovic et al.   NEUROBIOLOGY OF DISEASE

Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease

(2012) Haiqun Jia et al.   NEUROBIOLOGY OF DISEASE

Genetic Knock-Down of Hdac3 Does Not Modify Disease-Related Phenotypes in a Mouse Model of Huntington's Disease

(2012) Lara Moumné et al.   PLoS One

HDAC3 Is a Critical Negative Regulator of Long-Term Memory Formation

(2011) S. C. McQuown et al.   JOURNAL OF NEUROSCIENCE

Spinocerebellar Ataxia Type 7 Cerebellar Disease Requires the Coordinated Action of Mutant Ataxin-7 in Neurons and Glia, and Displays Non-Cell-Autonomous Bergmann Glia Degeneration

(2011) S. A. Furrer et al.   JOURNAL OF NEUROSCIENCE

Selective Toxicity by HDAC3 in Neurons: Regulation by Akt and GSK3 

(2011) F. H. Bardai et al.   JOURNAL OF NEUROSCIENCE

Lobule-specific membrane excitability of cerebellar Purkinje cells

(2011) Chang-Hee Kim et al.   JOURNAL OF PHYSIOLOGY-LONDON

Vascular endothelial growth factor ameliorates the ataxic phenotype in a mouse model of spinocerebellar ataxia type 1

(2011) Marija Cvetanovic et al.   NATURE MEDICINE

Histone Deacetylase 3 Depletion in Osteo/Chondroprogenitor Cells Decreases Bone Density and Increases Marrow Fat

(2010) David F. Razidlo et al.   PLoS One

Histone deacetylase (HDAC) inhibitors in recent clinical trials for cancer therapy

(2010) Julia M. Wagner et al.   Clinical Epigenetics

Putting the ‘HAT’ back on survival signalling: the promises and challenges of HDAC inhibition in the treatment of neurological conditions

(2009) Sama F Sleiman et al.   EXPERT OPINION ON INVESTIGATIONAL DRUGS

Haploinsufficiency of AFG3L2, the Gene Responsible for Spinocerebellar Ataxia Type 28, Causes Mitochondria-Mediated Purkinje Cell Dark Degeneration

(2009) F. Maltecca et al.   JOURNAL OF NEUROSCIENCE

Cerebellar cortical organization: a one-map hypothesis

(2009) Richard Apps et al.   NATURE REVIEWS NEUROSCIENCE

Liver-specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks

(2008) Sarah K Knutson et al.   EMBO JOURNAL

Pathogenic Mechanisms of a Polyglutamine-mediated Neurodegenerative Disease, Spinocerebellar Ataxia Type 1

(2008) Huda Y. Zoghbi et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Maintenance of cardiac energy metabolism by histone deacetylase 3 in mice

(2008) Rusty L. Montgomery et al.   JOURNAL OF CLINICAL INVESTIGATION

Deletion of Histone Deacetylase 3 Reveals Critical Roles in S Phase Progression and DNA Damage Control

(2008) Srividya Bhaskara et al.   MOLECULAR CELL

The insulin-like growth factor pathway is altered in spinocerebellar ataxia type 1 and type 7

(2008) J. R. Gatchel et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice

(2008) E. A. Thomas et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA