HDAC1, FLAG-Tag, His-Tag Recombinant

Catalog #
50051
$485 *
Size: 50 µg
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Description

Human recombinant HDAC1 (Histone deacetylase 1), full length, encompassing amino acids 1-482(end). This construct contains a C-terminal His-tag (6xHis) followed by a FLAG-tag. This recombinant protein was affinity purified as a complex with endogenous tubulin.

This product has been cited 159 times.

Synonyms
Histone deacetylase 1, HD1, Protein deacetylase HDAC1, Protein decrotonylase HDAC1, RPD3L1
Product Info
Storage and Usage
Citations159
Species
Human
Construct
HDAC1/Tubulin (1-482(end)-His-FLAG)
Host Species/Expression System
Sf9
Purity

≥90%

Format

Aqueous buffer solution.

Formulation

40 mM Tris-HCl, pH 8.0, 110 mM NaCl, 2.2 mM KCl, 100 ng/µl FLAG peptide, and 20% Glycerol

MW
56 kDa + Tubulin (55 kDa)
Amino Acids
1-482(end)
Specific Activity

460 pmol/min/µg.

Genbank #
NM_004964
UniProt #
Q13547
Tag(s)
C-terminal His-tag, C-terminal FLAG-tag
Background

HDAC1, or histone deacetylate 1, is a Class I member of the histone deacetylase family which is involved in lysine deacetylation. Lysine acetylation/deacetylation is a dynamic process involved in the regulation of a variety of cellular functions, similarly to phosphorylation/dephosphorylation. HDAC1 is part of the histone deacetylase complex, localized in the nucleus, and regulates eukaryotic gene expression. It can also directly interact with different transcription factors to regulate specific pathways, for example: HDAC1 interacts with MTA-2 (metastasis-associated protein-2) to deacetylate p53 and thus participates in cell growth and apoptosis regulation. In endothelial cells HDAC regulates angiogenesis, inflammation, redox and nitric oxide signaling, in response to environmental stimuli. Dysfunction of HDAC1 can contribute to atherosclerosis. Mutations in HDAC1 can result in cancer, via the deregulation of genes involved in cell proliferation and survival. A number of HDAC inhibitors have been approved for the treatment of cancer, but most are non-selective. Entinostat (or MS-275) is an inhibitor that acts preferentially on HDAC1 and has shown promising results in phase I clinical trials for refractory solid tumors and lymphoma.  The development of new inhibitors specifically targeting HDAC1 may open newer avenues for cancer and HDAC1-linked diseases in the endothelium.