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EMU191511

Sigma-Aldrich

MISSION® esiRNA

targeting mouse Hdac9

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About This Item

UNSPSC Code:
41105324
NACRES:
NA.51

description

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Quality Level

product line

MISSION®

form

lyophilized powder

esiRNA cDNA target sequence

TAGCAGCTCTCCAGGGTCAGGTCCCAGTTCACCAAACAATGGCCCTGCTGGGAATGTGACCGAAAATGAGGCTTCAGCTCTGCCTCCCACGCCTCACCCCGAGCAACTGGTTCCACAGCAGCGCATACTAATTCATGAAGATTCCATGAACCTGCTAAGTCTCTATACCTCCCCGTCCCTGCCCAATATCACTCTGGGACTTCCAGCAGTGCCGTCCCCACTCAATGCTTCTAACTCACTCAAAGACAAACAGAAGTGCGAGACACAGATGCTCAGACAAGGTGTTCCTCTGCCCAGTCAGTATGGCAGTAGCATTGCAGCGTCCTCCAGCCACGTTCATGTAGCAATGGAAGGAAAACCCACCAGCAGCCACCAGGCTCTCCTGCAGCACCTACTGCTGAAGGAACAAATGCGACAGCAAAAGCTTCTCGTGGCTGGTGGAGTTCCATTACACCCTCAGTCTCCTTTGGCAACAAAAGAAAGAATTTCACCAGGCATTAGAGGTACCCACAAATTGCC

Ensembl | mouse accession no.

NCBI accession no.

shipped in

ambient

storage temp.

−20°C

Gene Information

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 Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Dong-Qin Chen et al.
Oncotarget, 5(10), 3333-3349 (2014-05-17)
Chemoresistance is one of the most significant obstacles in lung adenocarcinoma (LAD) treatment, and this process involves genetic and epigenetic dysregulation of chemoresistance-related genes. Previously, we have shown that restoration of microRNA (miR)-200b significantly reverses chemoresistance of human LAD cells
Rui Yang et al.
Oncotarget, 6(10), 7644-7656 (2015-03-12)
Histone deacetylase 9 (HDAC9), a member of class II HDACs, regulates a wide variety of normal and abnormal physiological functions. We found that HDAC9 is over-expressed in prognostically poor glioblastoma patients. Knockdown HDAC9 decreased proliferation in vitro and tumor formation

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