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EPI007

Sigma-Aldrich

Histone Deacetylase 8 (HDAC8) Inhibitor Screening Kit

100 assays in 96 well plates

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Enzyme Commission number:
NACRES:
NA.41

usage

100 assays in 96 well plates

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... HDAC8(55869)
mouse ... HDAC8(70315)

Related Categories

General description

Histone deacetylases (HDACs) are a large family of enzymes that remove acetyl groups from histone proteins. Site specific histone acetylation and deacetylation have been shown to activate or repress eukaryotic gene transcription, respectively, and as a consequence, HDACs play a crucial role in mammalian development and disease. HDACs are involved in important biological activities, such as cell differentiation, proliferation, apoptosis, and senescence.

With Sigma′s HDAC8 Inhibitor Screening Kit, HDAC8 Enzyme acts with the supplied Developer to deacetylate and then cleave the HDAC8 Substrate (R-H-K(Ac)-K(Ac)-AFC). This activity releases the quenched fluorescent group, AFC, which can be detected at Em/Ex=380/500 nm. In the presence of a HDAC8 inhibitor, AFC is not released and its fluorescence remains quenched. The kit provides a rapid, simple, sensitive, and reliable test, suitable for either individual tests or high throughput screening of HDAC8 inhibitors. Trichostatin A (TSA) is included as a control inhibitor to compare with the efficacy of test inhibitors.

Features and Benefits

  • Simple, sensitive, and reliable assay
  • Simple procedure; takes ~60 min
  • Utilizes fluorometric methods
  • Sample type: candidate HDAC8 inhibitors
  • Suitable for screening HDAC8 inhibitors
  • Suitable for individual tests or high throughput assays
  • Convenient 96-well microplate format

Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

188.6 °F - closed cup

Flash Point(C)

87 °C - closed cup

Regulatory Information

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Q Yang et al.
Cell proliferation, 46(6), 654-664 (2014-01-28)
Pulmonary arterial hypertension, characterized by pulmonary vascular remodelling and vasoconstriction, is associated with excessive proliferative changes in pulmonary vascular walls. However, the role of HDACs in the phenotypic alteration of pulmonary arterial smooth muscle cells (PASMC) is largely unknown. Pulmonary
Li-Sophie Z Rathje et al.
Proceedings of the National Academy of Sciences of the United States of America, 111(4), 1515-1520 (2014-01-30)
Oncogenes deregulate fundamental cellular functions, which can lead to development of tumors, tumor-cell invasion, and metastasis. As the mechanical properties of cells govern cell motility, we hypothesized that oncogenes promote cell invasion by inducing cytoskeletal changes that increase cellular stiffness.
Hai-Ying Zhu et al.
Biochemical and biophysical research communications, 444(4), 638-643 (2014-02-05)
Interspecies somatic cell nuclear transfer (iSCNT) is a promising method to clone endangered animals from which oocytes are difficult to obtain. Monomeric red fluorescent protein 1 (mRFP1) is an excellent selection marker for transgenically modified cloned embryos during somatic cell
Bihua Bie et al.
Nature neuroscience, 17(2), 223-231 (2014-01-21)
Amyloid-induced microglial activation and neuroinflammation impair central synapses and memory function, although the mechanism remains unclear. Neuroligin 1 (NLGN1), a postsynaptic protein found in central excitatory synapses, governs excitatory synaptic efficacy and plasticity in the brain. Here we found, in
Yong Wang et al.
Circulation research, 114(6), 957-965 (2014-01-31)
Our previous study has shown that yes-associated protein (YAP) plays a crucial role in the phenotypic modulation of vascular smooth muscle cells (SMCs) in response to arterial injury. However, the role of YAP in vascular SMC development is unknown. The

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