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EMU002961

Sigma-Aldrich

MISSION® esiRNA

targeting mouse Pvrl1

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About This Item

UNSPSC Code:
41105324
NACRES:
NA.51

description

Powered by Eupheria Biotech

product line

MISSION®

form

lyophilized powder

esiRNA cDNA target sequence

GGCCATCTACAACCCGACTATGGGTGTGTCCGTGCTGCCTCCCTACGAGAAACGAGTGGAGTTCCTGCGACCCTCCTTCATCGACGGCACCATCCGCCTCTCCGGTCTGGAGCTGGAGGACGAGGGCATGTACATCTGTGAATTTGCCACCTTCCCTACGGGCAACCGTGAAAGCCAGCTCAATCTCACTGTGATGGCCAAACCCACCAACTGGATTGAGGGCACCCGGGCGGTGCTTCGAGCCAGGAAGGGACAGGATGACAAGGTTTTGGTGGCCACCTGCACCTCAGCCAATGGGAAGCCTCCCAGTGCGGTGTCCTGGGAAACACGGCTAAAGGGCGAGGCAGAGTACCAGGAAATTCGGAACCCCAATGGCACCGTGACAGTCATCAGCCGTTACCGTTT

Ensembl | mouse accession no.

ENSMUSG00000032012

NCBI accession no.

NM_021424

shipped in

ambient

storage temp.

−20°C

Gene Information

mouse ... PVRL1(58235) , Pvrl1(58235)

General description

MISSION® esiRNA are endoribonuclease prepared siRNA. They are a heterogeneous mixture of siRNA that all target the same mRNA sequence. These multiple silencing triggers lead to highly-specific and effective gene silencing.

For additional details as well as to view all available esiRNA options, please visit SigmaAldrich.com/esiRNA.

Legal Information

MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

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Joseph C K Leung et al.
Apoptosis : an international journal on programmed cell death, 20(7), 907-920 (2015-03-27)
Glomerulo-podocytic communication plays an important role in the podocytic injury in IgA nephropathy (IgAN). In this study, we examine the role of podocytic angiotensin II receptor subtype 1 (AT1R) and prorenin receptor (PRR) in podocytic apoptosis in IgAN. Polymeric IgA
Feng Y Liu et al.
Journal of the renin-angiotensin-aldosterone system : JRAAS, 15(2), 99-108 (2014-03-05)
Since the discovery of the (pro)renin receptor (PRR), it has been considered as a novel bioactive molecule of the renin-angiotensin system (RAS). The activation of PRR can elicit a series of angiotensin II (AngII)-independent effects. In this study, we investigated
Caixia Li et al.
American journal of physiology. Endocrinology and metabolism, 309(3), E302-E310 (2015-06-18)
High glucose reduces autophagy and enhances apoptosis of podocytes. Previously, we reported that high glucose induced podocyte injury through upregulation of the (pro)renin receptor (PRR). We hypothesized that increasing PRR reduces autophagy and increases apoptosis of mouse podocytes exposed to

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