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EHU132211

Sigma-Aldrich

MISSION® esiRNA

targeting human PDE6D

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About This Item

UNSPSC Code:
41105324
NACRES:
NA.51

description

Powered by Eupheria Biotech

Quality Level

100

product line

MISSION®

form

lyophilized powder

esiRNA cDNA target sequence

GACCTGTCTGTCCCTGGTGTGGAGCATGAAGCCCGTGTTCCCAAGAAAATCCTCAAGTGCAAGGCAGTGTCTCGAGAACTTAATTTTTCTTCGACAGAACAAATGGAAAAATTCCGCCTGGAACAAAAAGTTTACTTCAAAGGGCAATGCCTAGAAGAATGGTTCTTCGAGTTTGGCTTTGTGATCCCTAACTCCACAAATACCTGGCAGTCCTTGATAGAGGCAGCACCCGAGTCCCAGATGATGCCAGCAAGCGTCTTAACTGGGAACGTTATCATAGAAACAAAGTTTTTTGACGACGATCTTCTTGTAAGCACATCCAGAGTGAGACTTTTCTATGTTTGAAAGAAGAATGTGTGTACATTTCAAGAATTTGGGTTTTTTGGAGGGAGGAGGAAACT

Ensembl | human accession no.

ENSG00000156973

NCBI accession no.

NM_002601

shipped in

ambient

storage temp.

−20°C

Gene Information

human ... PDE6D(5147) , PDE6D(5147)

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

Certificates of Analysis (COA)

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Sevdalina Nikolova et al.
Respiratory research, 11, 146-146 (2010-10-29)
Idiopathic Pulmonary Fibrosis (IPF) is an unresolved clinical issue. Phosphodiesterases (PDEs) are known therapeutic targets for various proliferative lung diseases. Lung PDE6 expression and function has received little or no attention. The present study aimed to characterize (i) PDE6 subunits
Michael Dumbacher et al.
Molecular neurodegeneration, 13(1), 50-50 (2018-09-28)
Neuronal Ca2+ dyshomeostasis and hyperactivity play a central role in Alzheimer's disease pathology and progression. Amyloid-beta together with non-genetic risk-factors of Alzheimer's disease contributes to increased Ca2+ influx and aberrant neuronal activity, which accelerates neurodegeneration in a feed-forward fashion. As

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