EPI007
Histone Deacetylase 8 (HDAC8) Inhibitor Screening Kit
100 assays in 96 well plates
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About This Item
Produits recommandés
Utilisation
100 assays in 96 well plates
Numéro d'accès NCBI
Conditions d'expédition
wet ice
Température de stockage
−20°C
Informations sur le gène
human ... HDAC8(55869)
mouse ... HDAC8(70315)
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.
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.
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.
Caractéristiques et avantages
- 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
Produit(s) apparenté(s)
Réf. du produit
Description
Tarif
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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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
Astrid M Kral et al.
Biochemistry, 53(4), 725-734 (2014-01-24)
Histone deacetylases (HDACs) play diverse roles in many diseases including cancer, sarcopenia, and Alzheimer's. Different isoforms of HDACs appear to play disparate roles in the cell and are associated with specific diseases; as such, a substantial effort has been made
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
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