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EPI005

Sigma-Aldrich

Histone Deacetylase 3 (HDAC3) Inhibitor Screening Kit

100 assays in 96 well plates

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About This Item

Numéro de classification (Commission des enzymes):
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.41

Utilisation

100 assays in 96 well plates

Conditions d'expédition

dry ice

Température de stockage

−20°C

Informations sur le gène

human ... HDAC3(8841)
mouse ... HDAC3(15183)

Description générale

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. Of the several classes of HDACs, this kit assays a member of the zinc-independent, NADH requiring class, HDAC3. With Sigma′s HDAC3 Inhibitor Screening Kit, HDAC3 Enzyme acts with the supplied Developer to deacetylate and then cleave the HDAC3 Substrate [Arg-His-Lys-Lys(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 HDAC3 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 HDAC3 inhibitors. Trichostatin A (TSA) is included as a control inhibitor to compare with the efficacy of test inhibitors.

Caractéristiques et avantages

  • Simple, sensitive, and reliable assay
  • Simple procedure; takes ~60 min
  • Utilizes fluorometric methods
  • Sample type: candidate HDAC3 inhibitors
  • Suitable for screening HDAC3 inhibitors
  • Suitable for individual tests or high throughput assays and kinetic studies
  • Convenient 96-well microplate format

Autres remarques

The kit is shipped on dry ice. Store HDAC-3 enzyme at -80 °C upon receipt. All other components should be stored at -20 °C, protected from light. All -20 °C reagents should be used within 2 months after thawing.

Produit(s) apparenté(s)

Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

188.6 °F - closed cup

Point d'éclair (°C)

87 °C - closed cup


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Consulter la Bibliothèque de documents

Ouafa Zerzaihi et al.
Biochemistry and cell biology = Biochimie et biologie cellulaire, 92(1), 61-67 (2014-01-30)
Besides its direct metabolic effects, insulin induces transcriptional alterations in its target tissues. However, whether such changes are accompanied by epigenetic changes on the chromatin template encompassing insulin responsive genes is unclear. Here, mRNA levels of insulin-responsive genes hexokinase 2
Johannes Gräff et al.
Cell, 156(1-2), 261-276 (2014-01-21)
Traumatic events generate some of the most enduring forms of memories. Despite the elevated lifetime prevalence of anxiety disorders, effective strategies to attenuate long-term traumatic memories are scarce. The most efficacious treatments to diminish recent (i.e., day-old) traumata capitalize on memory updating
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
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
Ji Heon Noh et al.
Cancer research, 74(6), 1728-1738 (2014-01-23)
Aberrant regulation of histone deacetylase 2 (HDAC2) contributes to malignant progression in various cancers, but the underlying mechanism leading to the activation of oncogenic HDAC2 remains unknown. In this study, we show that HDAC2 expression is upregulated in a large

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