This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
Immunogen
This HDAC4 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1052-1084 amino acids from the C-terminal region of human HDAC4.
HDAC4
Reactivity: Human
WB, ELISA
Host: Rabbit
Polyclonal
unconjugated
Application Notes
WB: 1:1000
Restrictions
For Research Use only
Format
Liquid
Buffer
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C,-20 °C
Storage Comment
Maintain refrigerated at 2-8 °C for up to 6 months. For long term storage store at -20 °C in small aliquots to prevent freeze-thaw cycles.
Expiry Date
6 months
Target
HDAC4
(Histone Deacetylase 4 (HDAC4))
Alternative Name
HDAC4
Background
DNA is wrapped around histone proteins to form nucleosomes and chromatin fiber, a higher-order structure. Chromatin can become alternatively revealed to or concealed from transcription factors. Acetylation of lysine residues induces conformational changes in core histones by destabilizing nucleosomes and allowing transcription factors access to recognition elements in DNA. Deacetylation of histones by histone deacetylases (HDACs) reseals the chromosomal package, leading to a repression of transcription. HDAC4 does not bind DNA directly, but rather through MEF2C and MEF2D. Binding of the N terminus of HDAC4 to MEF2C represses MEF2C transcription activity. The catalytic domain of HDAC4 interacts with HDAC3 via the transcriptional corepressor NCOR2. Experimental conditions leading to the suppression of HDAC4 binding to NCOR2 and to HDAC3 result in loss of enzymatic activity associated with HDAC4, indicating regulation of transcription by bridging the enzymatically active NCOR2-HDAC3 complex and select transcription factors. HDAC4 and MITR contain calmodulin-binding domains that overlap with their MEF2 binding domains. Binding of calmodulin to HDAC4 leads to its dissociation from MEF2, relieving MEF2 from the transcriptional repression by HDAC4. Together, HDAC4, MITR, and CABIN1 constitute a family of calcium-sensitive transcriptional repressors of MEF2. In murine studies, HDAC4, which is expressed in prehypertrophic chondrocytes, interacts with and inhibits the activity of Runx2 in mice, a transcription factor necessary for chondrocyte hypertrophy, establishing HDAC4 as a central regulator of chondrocyte hypertrophy and skeletogenesis.