추천 제품
사용
100 assays in 96 well plates
NCBI 수납 번호
배송 상태
dry ice
저장 온도
−20°C
유전자 정보
human ... HDAC3(8841)
mouse ... HDAC3(15183)
일반 설명
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.
특징 및 장점
- 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
기타 정보
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.
관련 제품
제품 번호
설명
가격
Storage Class Code
10 - Combustible liquids
WGK
WGK 3
Flash Point (°F)
188.6 °F - closed cup
Flash Point (°C)
87 °C - closed cup
가장 최신 버전 중 하나를 선택하세요:
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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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