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Merck
CN

EHU154011

MISSION® esiRNA

targeting human SDC4

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关于此项目

NACRES:
NA.51
UNSPSC Code:
41105324
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description

Powered by Eupheria Biotech

product line

MISSION®

form

lyophilized powder

esiRNA cDNA target sequence

CCACCGAACCCAAGAAACTAGAGGAGAATGAGGTTATCCCCAAGAGAATCTCACCCGTTGAAGAGAGTGAGGATGTGTCCAACAAGGTGTCAATGTCCAGCACTGTGCAGGGCAGCAACATCTTTGAGAGAACGGAGGTCCTGGCAGCTCTGATTGTGGGTGGCATCGTGGGCATCCTCTTTGCCGTCTTCCTGATCCTACTGCTCATGTACCGTATGAAGAAGAAGGATGAAGGCAGCTATGACCTGGGCAAGAAACCCATCTACAAGAAAGCCCCCACCAATGAGTTCTACGCGTGAAGCTTGCTTGTGGGCACTGGCTTGGACTTTAGCGGGGAGGGAAGCCAGGGGATTTTGAAGGGTGGACATTAGGGTAGGGTGAGGTCAACCTAATACTGACTTGTCAGTATCTCCAGCTCTGATTACCTTTGAAGTGTTCAGAAGAGACATTGTCTTCTACTGTTCTGCCAGGTTCTTCTTGAGCTTTGGGCCTCAGTTGCCCTGGCAGAAAAATGGATTCAACTTGGCCTTTCTGAAGGCAAGACTGGGAT

Ensembl | human accession no.

NCBI accession no.

shipped in

ambient

storage temp.

−20°C

Quality Level

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

存储类别

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

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Bernadien M Nijmeijer et al.
Frontiers in immunology, 11, 503-503 (2020-04-16)
Sexually transmitted Hepatitis C virus (HCV) infections and high reinfections are a major concern amongst men who have sex with men (MSM) living with HIV-1 and HIV-negative MSM. Immune activation and/or HIV-1 coinfection enhance HCV susceptibility via sexual contact, suggesting
Zhe Xie et al.
Cell death and differentiation, 25(8), 1442-1456 (2018-01-21)
Dysregulation of Wnt signaling has been implicated in developmental defects and in the pathogenesis of many diseases such as osteoarthritis; however, the underlying mechanisms are poorly understood. Here, we report that non-canonical Wnt signaling induced loss of chondrocyte phenotype through
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