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FLASH GENE

Symbol

HDAC1

contributors: mct/shn/ - updated : 06-11-2018

HGNC name	histone deacetylase 1
HGNC id	4852

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   overexpressed in rheumatoid arthritis synovial fibroblasts (RA-SF), supporting cell proliferation and survival of RA-SF but suppressing MMP1 production constitutional         loss of HDAC1, but not HDAC2, reduces the level of HDAC activity associated with HDAC1/2 complexes and leads to the enhanced differentiation of embryoid bodies tumoral     --low   is linked to enhanced tumour malignancy constitutional     --over   led to senescence through both an accumulation of hypophosphorylated active retinoblastoma protein (RB1) and an increase in the protein level of protein phosphatase 2A catalytic subunit (PPP2CA)

Susceptibility

Variant & Polymorphism

Candidate gene
Marker	presence of HDAC1 could provide a biomarker for benign teratomas
Therapy target
	System Type Disorder Pubmed cancer     induced premature senescence by HDAC1 overexpression may be a powerful tumor-suppressor mechanism for use in cancer therapy blood hemoglobin   potential of isoform-selective inhibitors of HDAC1 and HDAC2 for the treatment of sickle cell disease

ANIMAL & CELL MODELS

	mice with conditional Hdac1 null alleles die by embryonic day 9.5
	Cardiac-specific deletion of HDAC1 and HDAC2 genes results in neonatal lethality with cardiac arrhythmias, dilated cardiomyopathy, and up-regulation of genes encoding skeletal muscle-specific contractile proteins and calcium channels
	deletion of both HDAC1 and HDAC2 genes in mouse developing neurons results in severe hippocampal abnormalities, absence of cerebellar foliation, disorganization of cortical neurons, and lethality by postnatal day 7
	ablation of Hdac1 and Hdac2 specifically in mouse Schwann cells, result in massive Schwann cell loss and virtual absence of myelin in mutant sciatic nerves (