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Merck

EPI005

Sigma-Aldrich

Histone Deacetylase 3 (HDAC3) Inhibitor Screening Kit

100 assays in 96 well plates

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About This Item

Enzyme Commission szám:
UNSPSC kód:
12352200
NACRES:
NA.41

használat

100 assays in 96 well plates

kiszállítva

dry ice

tárolási hőmérséklet

−20°C

Géninformáció

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

Általános leírás

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.

Tulajdonságok és előnyök

  • 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

Egyéb megjegyzések

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.

kapcsolódó termék

Product No.
Leírás
Árazás

Tárolási osztály kódja

10 - Combustible liquids

WGK

WGK 3

Lobbanási pont (F)

188.6 °F - closed cup

Lobbanási pont (C)

87 °C - closed cup


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Analitikai tanúsítványok (COA)

Lot/Batch Number

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Dokumentumtár megtekintése

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
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
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
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.

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