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EPI004

Sigma-Aldrich

Histone Deacetylase 3 (HDAC3) Activity Assay Kit

100 assays in 96 well plates

Synonyme(s) :

Histone deacetylase assay

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About This Item

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

Utilisation

100 assays in 96 well plates

Conditions d'expédition

wet 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, it plays 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 HDAC3 Activity Assay Kit, HDAC3 present in a test sample will act with the supplied Developer, to deacetylate and then cleave the HDAC3 Substrate [R-H-K-K(Ac)-AFC]. This activity will release the quenched fluorescent group, AFC, which can be detected at Em/Ex = 380/500 nm. Trichostatin A is an HDAC inhibitor included in the kit to verify HDAC3 activity. The kit provides a rapid, simple, sensitive and reliable test. It is suitable for either individual tests or high throughput assays, from nuclear extracts, purified, or immunoprecipitated HDAC3, and from native, recombinant, or genetically modified HDAC3.

Caractéristiques et avantages

  • Simple, sensitive, and reliable assay
  • Simple procedure; takes ~60 min
  • Utilizes fluorometric methods
  • Sample type: cell and tissue lysates, plasma and serum, other biological fluids
  • Species reactivity: mammalian
  • Suitable for individual tests or high throughput assays and kinetic studies
  • Convenient 96-well microplate format
  • Suitable for high throughput measurement of HDAC3 activity in purified, immunoprecipitated and recombinant or genetically modified HDAC3 samples

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

Karolina J Janczura et al.
Proceedings of the National Academy of Sciences of the United States of America, 115(47), E11148-E11157 (2018-11-07)
Alzheimer's disease (AD) is the leading cause of age-related dementia. Neuropathological hallmarks of AD include brain deposition of β-amyloid (Aβ) plaques and accumulation of both hyperphosphorylated and acetylated tau. RGFP-966, a brain-penetrant and selective HDAC3 inhibitor, or HDAC3 silencing, increases
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
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.
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
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

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