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CS1040

Sigma-Aldrich

SIRT1 Assay Kit

sufficient for 100 assays

Synonyme(s) :

SIRT1 Activity Assay

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About This Item

Code UNSPSC :
12161503
Nomenclature NACRES :
NA.84

Utilisation

sufficient for 100 assays

Niveau de qualité

Conditions d'expédition

dry ice

Température de stockage

−20°C

Informations sur le gène

human ... SIRT1(23411)

Description générale

The SIRT1 Assay Kit offers all the reagents required for the measurement of purified SIRT1 activity and for screening of inhibitors/activators.
The assay procedure is based on a two-step enzymatic reaction. The first step is deacetylation by SIRT1 of a substrate that contains an acetylated lysine side chain. The second step is the cleavage of the deacetylated substrate by the Developing Solution and the release of a highly fluorescent group. The measured fluorescence is directly proportional to the deacetylation activity of the enzyme in the sample.

Application

SIRT1 Assay Kit has been used in measuring the Sirt1 deacetylase activity in mesenchymal stem cells (MSCs), human retinal endothelial cells (HRECs) and human neuroblastoma SH-SY5Y cells.

Actions biochimiques/physiologiques

Sirtuins (Sir2) are an evolutionarily conserved family of NAD+ dependent histone/protein deacetylases that tightly couple the cleavage of NAD+ and the deacetylation of protein substrates. The reaction products are nicotinamide, the deacetylated product, and a novel metabolite, 2′-O-acetyl-ADP-ribose. The proteins within this family are named after the first protein discovered from this family, Sir2 (Silent Information Regulator 2). Besides gene silencing, sirtuin proteins are important in other processes such as cell cycling regulation and fatty acid metabolism. SIRT1 is the human homolog of Sir2 and the one most studied to date. SIRT1 mediates p53 dependent process, transcription regulation, muscle differentiation, adipogenesis, and protection from axonal degeneration. SIRT1 also participates in early embryogenesis, neurogenesis, and cardiogenesis.

Caractéristiques et avantages

The kit offers all the reagents required for the fast and easy measurement of purified SIRT1 activity and for screening of inhibitors/activators. Moreover, the kit contains an inhibitor (nicotinamide) and an activator (resveratrol) as negative and positive controls, respectively.

Composants de kit également disponibles séparément

Réf. du produit
Description
FDS

  • SIRT1 Substrate (Fluorometric) 100 μL

  • Developer Solution 1.5 mL

  • S8446SIRT1 human, recombinant, expressed in E. coli, N-terminal histidine tagged, ≥90% (SDS-PAGE), buffered aqueous glycerol solution 150 μgFDS

  • NAD+ Solution 1 mL

Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

188.6 °F

Point d'éclair (°C)

87 °C


Certificats d'analyse (COA)

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Les clients ont également consulté

Nicotinamide phosphoribosyltransferase (Nampt) affects the lineage fate determination of mesenchymal stem cells: a possible cause for reduced osteogenesis and increased adipogenesis in older individuals
Li Y, et al.
Journal of Bone and Mineral Research, 26(11), 2656-2664 (2011)
Fenofibrate suppresses cellular metabolic memory of high glucose in diabetic retinopathy via a sirtuin 1-dependent signalling pathway
Zhao S, et al.
Molecular Medicine Reports, 12(4), 6112-6118 (2015)
Flávia Gerelli Ghiraldini et al.
Molecular biology of the cell, 24(15), 2467-2476 (2013-06-14)
Hyperglycemia, like aging, induces chromatin remodeling in mouse hepatocytes in comparison to normoglycemia and younger age, respectively. Changes in glucose metabolism also affect the action and expression of sirtuins, promoting changes in chromatin conformation and dynamics. Here we investigate the
Haiyan Chu et al.
American journal of respiratory cell and molecular biology, 58(1), 28-39 (2017-08-12)
Pulmonary fibrosis is the leading cause of death in systemic sclerosis (SSc). Sirtuin1 (SIRT1) is a deacetylase with known antiinflammatory and antifibrotic activity in the liver, kidney, and skin. The role of SIRT1 in SSc-related pulmonary fibrosis is unknown. In
Kai Le et al.
International immunopharmacology, 75, 105779-105779 (2019-07-31)
Neonatal hypoxic-ischemic brain injury (HIBI) is a knotty disease that lacks appropriate treatment. Inflammation is an important contributor to brain damage, and microglia are responsible for eliciting early and pronounced inflammatory reactions in the immature brain after hypoxic-ischemic (HI) insult.

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