Assay-kits

SensoLyte® 520 Renin Assay Kit Fluorimetric - 1 kit

$687.00
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  • Cat.Number : AS-72040
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    In stock
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Renin, a highly specific aspartyl protease, cleaves angiotensinogen, to yield angiotensin I, which is further converted into angiotensin II by ACE (Angiotensin Converting Enzyme). Angiotensin II constricts blood vessels leading to increased blood pressure. It also increases the secretion of ADH and aldosterone, and stimulates the hypothalamus to activate the thirst reflex. Since an overactive renin-angiotensin system leads to hypertension, renin is an attractive target for the treatment of this disease.
The SensoLyte® 520 Renin Assay Kit provides a convenient assay for high throughput screening of renin inhibitors and for continuous assay of renin activity using a 5-FAM/QXL™520 fluorescence resonance energy transfer (FRET) peptide. In the FRET peptide the fluorescence of 5-FAM is quenched by QXL™520. Upon cleavage into two separate fragments by renin, the fluorescence of 5-FAM is recovered, and can be monitored at excitation/emission = 490/520 nm. This assay is about fifty fold more sensitive than an EDANS/DABCYL-based assay and can detect 0.8 ng/ml renin.

Specifications

Packaging
Kits components
  • Component A: Renin substrate 5-FAM/QXL™520 FRET peptide Ex/Em=490 nm/520 nm upon cleavage: 1.5 mM DMSO solution, 50 µL Component B: 5-FAM, fluorescence reference standard: 1mM, 20 µL Component C: Human recombinant renin: 50 µL Component D: Assay buffer: 25 mL Component E: Renin Inhibitor Ac-HPFV- (Sta)-LF-NH2: 1mM DMSO solution, 4 µL
Chemistry
UniProt number
  • P00797
Properties
Absorbance (nm)
  • 490
Emission (nm)
  • 520
Storage & stability
Storage Conditions
  • Store component C at -80°C. Store all other components at -20°C. Component D can be stored at room temperature for convenience. Protect components A and B from light and moisture.
Activity
Application
Biomarker Target
Detection Method
Detection Limit
  • 0.8 ng/ml
Research Area
Sub-category Research Area
Usage
  • Research use
Source
Host

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Citations

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IQGAP1 regulates ERK1/2 and AKT signaling in the heart and sustains functional remodeling upon pressure overload

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High glucose upregulates upstream stimulatory factor 2 in human renal proximal tubular cells through angiotensin II-dependent activation of CREB

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  • N.P. Visavadiya

The (pro)renin receptor is cleaved by ADAM19 in the Golgi leading to its secretion into extracellular space.

Hypertens Res. . 2011 May 01 ; 34(5) 599 | DOI : 10.1038/hr.2010.284

  • A. Yoshikawa

Mechanism of VEGF expression by high glucose in proximal tubule epithelial cells

Mol Cell Endocrinol. . 2009 Sep 16 ; 314(1) 136 | DOI : 10.1016/j.mce.2009.09.009

  • D. Feliers

Direct renin inhibition improved insulin resistance and adipose tissue dysfunction in type 2 diabetic KK-A(y) mice.

J Hypertens . 2010 Jul 01 ; 28(7) 1471 | DOI : 10.1097/HJH.0b013e32833bc420

  • M. Iwai

Effects of renal autograft ischemic storage and reperfusion on intraoperative hemodynamic patterns and plasma renin concentrations in clinically normal cats undergoing renal autotransplantation and contralateral nephrectomy

Am J Vet Res. . 2010 Oct 01 ; 71(10) 1220 | DOI : 10.2460/ajvr.71.10.1220

  • C.W. Schmiedt

Expression of protein complex comprising the human prorenin and (pro)renin receptor in silkworm larvae using Bombyx mori nucleopolyhedrovirus (BmNPV) bacmids for improving biological function.

Mol Biotechnol . 2009 Jun 07 ; 43(2) 154 | DOI : 10.1007/s12033-009-9183-7

  • D. Du

Measurement of plasma renin concentration in cats by use of a fluorescence resonance energy transfer peptide substrate of renin

Am J Vet Res. . 2009 Nov 01 ; 70(11) 1315 | DOI : 10.2460/ajvr.70.11.1315

  • C.W. Schmiedt

Dominant renin gene mutations associated with early-onset hyperuricemia, anemia, and chronic kidney failure

Am J Hum Genet. . 2009 Aug 06 ; 85(2) 204 | DOI : 10.1016/j.ajhg.2009.07.010

  • M. Živná

Design, synthesis and biological evaluation of renin inhibitors guided by simulated annealing of chemical potential simulations.

Bioorg Med Chem. . 2017 Aug 01 ; 25(15) 3947 | DOI : 10.1016/j.bmc.2017.05.032

  • IS. Cloudsdale
  • et al