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EHU008921

Sigma-Aldrich

MISSION® esiRNA

targeting human MARCH5

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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

GCTGCAGCAGGAATAATGGTCGGCTCTATCTATTGGACAGCTGTGACTTATGGAGCAGTGACAGTGATGCAGGTTGTAGGTCATAAAGAAGGTCTGGATGTTATGGAGAGAGCTGATCCTTTATTCCTTTTAATTGGACTTCCTACTATTCCTGTCATGCTGATATTAGGCAAGATGATTCGCTGGGAGGACTATGTGCTTAGACTGTGGCGCAAATACTCGAATAAACTACAAATTTTAAATAGTATATTTCCAGGGATAGGTTGTCCTGTTCCTCGAATTCCAGCTGAGGCCAATCCTTTAGCAGATCATGTCTCTGCTACTCGAATCTTGTGTGGAGCCCTTGTCTTTCCTACTATTGCTACAATAGTTGGTAAATTGATGTTCAGTAGTGTTAACTCTAATTTACAAAGGACAATCTTGGGTGGAATTGC

Ensembl | human accession no.

ENSG00000198060

NCBI accession no.

NM_017824

shipped in

ambient

storage temp.

−20°C

Gene Information

human ... MARCH5(54708) , MARCH5(54708)

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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Linhe Lu et al.
Clinical and translational medicine, 10(5), e166-e166 (2020-10-01)
Myocardial ischemia/reperfusion (MI/R) injury imposes devastating cardiovascular sequelae in particular cardiac dysfunction as a result of restored blood flow. However, the mechanism behind MI/R injury remains elusive. Mitochondrial ubiquitin ligase (MITOL/MARCH5) is localized at the mitochondria-ER contact site and may
Young-Suk Yoo et al.
Nature communications, 6, 7910-7910 (2015-08-08)
Mitochondria serve as platforms for innate immunity. The mitochondrial antiviral signalling (MAVS) protein forms aggregates that elicit robust type-I interferon induction on viral infection, but persistent MAVS signalling leads to host immunopathology; it remains unknown how these signalling aggregates are

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