AnaSpec Expands SensoLyte® 520 Renin Assay Kits Collection

San Jose, CA, January 25, 2012 --(PR.com)-- AnaSpec, the provider of the ultra-sensitive SensoLyte® 520 Human Renin Assay Kit now provides renin kits specific for mouse and rat - the SensoLyte® 520 Mouse Renin Assay Kit and SensoLyte® 520 Rat Renin Assay Kit. Using their proprietary 5-FAM/QXL™ 520 fluorescence resonance energy transfer (FRET) peptide, all three assays are ideal for screening of renin inhibitors and for continuous assay of renin activity, especially for high throughput screening (HTS) purposes. In the intact FRET peptide, the fluorescence of 5-FAM is quenched by QXL™ 520. However, upon cleavage into two separate fragments by rat renin, the fluorescence of 5-FAM is recovered, and can be monitored at excitation/emission = 490/520 nm. With a high fluorescence quantum yield and long emission wavelength, the signal of 5-FAM can be detected with less interference from the autofluorescence of cell components and test compounds. The assays are performed in a convenient 96-well microplate format and can be adjusted to 384-well microplate format.

Key characters for SensoLyte® 520 Renin Assay Kits are ultra-sensitive, detects long wavelength and minimal autoflorescence, with FRET based substrates, and specific for human, mouse and rat.

The renin–angiotensin system (RAS) plays a central role in the regulation of blood pressure and electrolyte homoeostasis.1 At the first and rate-limiting step of the RAS cascade, renin, a highly specific aspartyl protease, cleaves angiotensinogen, produced in the liver, 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. 2-4

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References:
1. He, FJ. and GA. MacGregor, J. Renin Angiotensin Aldosterone Syst. 4, 11 (2003).
2. Wood, JM. et al., Hypertension, 7, 797 (1985).
3. Shibasaki, M. et al., Am. J. Hypertens. 4, 932 (1991).
4. Wood, JM.et al., Biochem. Biophys. Res. Comm. 308, 698 (2003).

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