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Merck

CS1090

HMG-CoA Reductase Assay Kit

sufficient for 30 assays (1 mL), sufficient for 100 assays (200 μL)

Sinónimos:

HMGR Assay Kit

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NACRES:
NA.28
UNSPSC Code:
12161503
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usage

sufficient for 100 assays (200 μL), sufficient for 30 assays (1 mL)

shipped in

dry ice

storage temp.

−70°C

Quality Level

Gene Information

human ... HMGCR(3156)

Categorías relacionadas

General description

The HMG-CoA Reductase Assay Kit is an important tool for the basic research of cholesterol and other related metabolic pathways.

Application

The HMGR activity kit is designed for the detection of HMG-CoA reductase activity. A major function of the kit is to screen for various inhibitors and activators of the purified catalytic subunit of the enzyme, HMG-CoA reductase, which may play a crucial role in therapeutics. The assay is based on the spectrophotometric measurement of the decrease in absorbance at 340 nm, which represents the oxidation of NADPH by the catalytic subunit of HMGR in the presence of the substrate HMG-CoA.

Biochem/physiol Actions

HMGR (3-hydroxy-3-methylglutaryl-CoA reductase) is a transmembrane glycoprotein located on the endoplasmic reticulum. This enzyme catalyzes the four-electron reduction of HMG-CoA to coenzyme A (CoA) and mevalonate, which is the rate-limiting step in sterol biosynthesis. The activity of HMGR is controlled through synthesis, degradation, and phosphorylation in order to maintain the concentration of mevalonate derived products. In addition to the physiological regulation of HMGR, the human enzyme has been targeted successfully by drugs in the clinical treatment of high serum cholesterol levels. Controlling serum cholesterol levels has an important therapeutic role since hypercholesterolemia often leads to the development of atherosclerosis and subsequently to cardiovascular pathologies, which might result in myocardial infarction and stroke. It has been suggested that a disturbance of cholesterol homeostasis contributes to the development of a chronic inflammatory state.

Los componentes del kit también están disponibles por separado

Referencia del producto
Descripción
SDS

  • N6505β-Nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate, ≥95% (HPLC) 25 mgSDS

Clase de almacenamiento

10 - Combustible liquids

pictograms

Health hazardExclamation mark

signalword

Warning

hcodes

Hazard Classifications

Eye Irrit. 2 - STOT SE 2

target_organs

Eyes,Central nervous system

wgk

WGK 3


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  1. Which document(s) contains shelf-life or expiration date information for a given product?

    If available for a given product, the recommended re-test date or the expiration date can be found on the Certificate of Analysis.

  2. How do I get lot-specific information or a Certificate of Analysis?

    The lot specific COA document can be found by entering the lot number above under the "Documents" section.

  3. How do I find price and availability?

    There are several ways to find pricing and availability for our products. Once you log onto our website, you will find the price and availability displayed on the product detail page. You can contact any of our Customer Sales and Service offices to receive a quote.  USA customers:  1-800-325-3010 or view local office numbers.

  4. What is the Department of Transportation shipping information for this product?

    Transportation information can be found in Section 14 of the product's (M)SDS.To access the shipping information for this material, use the link on the product detail page for the product. 

  5. For Product CS1090, HMG-CoA Reductase Assay Kit, what is the concentration of kit component Product I5909, Pravastatin?

    The concentration of Pravastatin, Product I5909 in Product CS1090, HMG-CoA Reductase Assay Kit,  is 100 uM solution in assay buffer.

  6. What is the lowest concentration that you can use Pravastatin and observe inhibition in Product CS1090, HMG-CoA Reductase Assay kit?

    For Product CS1090, HMG-CoA Reductase Assay kit we do not observe any inhibition when using Pravastatin at 25 or 50 nM.  We observe inhibition of HMG-CoA Reductase with 250 nM pravastatin.

  7. My question is not addressed here, how can I contact Technical Service for assistance?

    Ask a Scientist here.

Mohammad Azizur Rahman et al.
BioMed research international, 2014, 828149-828149 (2014-06-25)
Oxidation of low-density lipoprotein (LDL) has been strongly suggested as the key factor in the pathogenesis of atherosclerosis. Mushrooms have been implicated in having preventive effects against chronic diseases due especially to their antioxidant properties. In this study, in vitro
Rosana Aparecida Manólio Soares et al.
International journal of molecular sciences, 16(2), 4150-4160 (2015-02-19)
The objective of this study was to identify the major peptides generated by the in vitro hydrolysis of Amaranthus cruentus protein and to verify the effect of these peptides on the activity of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase), a key enzyme
G A Holdgate et al.
Biochemical Society transactions, 31(Pt 3), 528-531 (2003-05-30)
The statins are inhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase (HMG-CoAR), and are utilized to decrease levels of atherogenic lipoproteins in patients with, or who are at high risk of, cardiovascular disease. This study describes the inhibition of a recombinant, catalytic
R Kleemann et al.
Current drug targets. Cardiovascular & haematological disorders, 5(6), 441-453 (2006-03-01)
Besides classical risk factors such as hypercholesterolemia and hypertension, chronic subacute inflammation has recently been recognized as an important force driving the development of atherosclerosis, the most common underlying cause of myocardial infarction and stroke. There is compelling evidence that
A J Koning et al.
Molecular biology of the cell, 7(5), 769-789 (1996-05-01)
In all eucaryotic cell types analyzed, proliferations of the endoplasmic reticulum (ER) can be induced by increasing the levels of certain integral ER proteins. One of the best characterized of these proteins is HMG-CoA reductase, which catalyzes the rate-limiting step

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