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3023

Sigma-Aldrich

AptaFluor® SAH Methyltransferase Assay

Synonyme(s) :

Methyltransferase Activity Assay

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481,00 €
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About This Item

Code UNSPSC :
41122100
Nomenclature NACRES :
NA.84

481,00 €

Check Cart for Availability
Devis pour commande en gros

Conditions d'expédition

dry ice

Température de stockage

−70°C

Description générale

The AptaFluor® SAH Methyltransferase TR-FRET Assay is a universal assay for enzymes that convert S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH), with a far-red, time-resolved Förster-resonance-energy-transfer (TR-FRET) readout. The assay can be used for all enzymes within the histone methyltransferase (HMT) and DNA methyltransferase (DNMT) families. The assay is designed specifically for high-throughput screening (HTS), with a simple mix-and-read format and 2 liquid addition steps. It is run in an endpoint mode: methyltransferase (MT) enzyme reactions are quenched with a universal stop reagent (provided) and then the detection reagents are added.

The assay offers reagent stability and compatibility with commonly used multimode plate readers. The AptaFluor® SAH Methyltransferase TR-FRET Assay provides the following benefits:
  • Simple, mix-and-read format ideal for HTS.
  • Robust MT detection under initial velocity conditions (=20% conversion of SAM to SAH).
  • Accommodates SAM concentrations as low as 100 nM and as high as 5 μM.
  • Far-red tracer further minimizes interference from fluorescent compounds and light scattering.

View full Transcreener® product list

Quantité

3023-B = 100 assay, 96-well
3023-1K = 1,000 assay, 384-well

Forme physique

Kit with buffered aqueous solutions

Informations légales

AptaFluor is a registered trademark of BellBrook Labs
Transcreener is a registered trademark of BellBrook Labs

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Certificats d'analyse (COA)

Lot/Batch Number
13791
13582
13581

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L Latini et al.
Cell death & disease, 5, e1404-e1404 (2014-09-05)
Spinal cord injury (SCI) is a devastating condition of CNS that often results in severe functional impairments for which there are no restorative therapies. As in other CNS injuries, in addition to the effects that are related to the primary
Kalyan C Kondapalli et al.
The Journal of biological chemistry, 287(43), 36239-36250 (2012-09-06)
Human NHA2, a newly discovered cation proton antiporter, is implicated in essential hypertension by gene linkage analysis. We show that NHA2 mediates phloretin-sensitive Na(+)-Li(+) counter-transport (SLC) activity, an established marker for hypertension. In contrast to bacteria and fungi where H(+)
Aileen K Sewell et al.
iScience, 25(5), 104186-104186 (2022-04-29)
The protein kinase complex target of rapamycin complex 1 (TORC1) is a critical mediator of nutrient sensing that has been widely studied in cultured cells and yeast, yet our understanding of the regulatory activities of TORC1 in the context of
Maria Teresa Viscomi et al.
Autophagy, 8(2), 222-235 (2012-01-18)
Autophagy is the evolutionarily conserved degradation and recycling of cellular constituents. In mammals, autophagy is implicated in the pathogenesis of many neurodegenerative diseases. However, its involvement in acute brain damage is unknown. This study addresses the function of autophagy in
Brian G Coon et al.
The Journal of cell biology, 208(7), 975-986 (2015-03-25)
Endothelial responses to fluid shear stress are essential for vascular development and physiology, and determine the formation of atherosclerotic plaques at regions of disturbed flow. Previous work identified VE-cadherin as an essential component, along with PECAM-1 and VEGFR2, of a
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