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EMU024081

Sigma-Aldrich

MISSION® esiRNA

targeting mouse Trim28

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UNSPSC Code:
41105324
NACRES:
NA.51

description

Powered by Eupheria Biotech

Quality Level

100

product line

MISSION®

form

lyophilized powder

esiRNA cDNA target sequence

TGATTCCCAGGATGCTAACCAGTGCTGCACTAGCTGTGAAGATAATGCCCCAGCCACTAGCTATTGTGTGGAGTGCTCTGAACCACTTTGTGAGACCTGTGTGGAGGCTCACCAGCGGGTGAAATACACCAAGGACCACACTGTGCGCTCCACAGGACCTGCTAAGACTCGAGATGGAGAGCGAACAGTCTACTGTAATGTGCACAAGCATGAGCCCCTCGTGCTGTTCTGTGAGAGCTGTGACACACTCACCTGCCGCGACTGCCAGCTCAACGCTCACAAGGACCATCAGTACCAGTTTTTGGAAGATGCAGTGAGGAACCAACGTAAACTCTTGGCTTCACTGGTGAAACGTCTTGGGGACAAACATGCCACACTTCAGAAAAACACCAAGGAGGTTCGAAGCTCGATCCGCCAGGTGTCTGATGTGCAGAAGCGAGTGCAGGTTGAT

Ensembl | mouse accession no.

ENSMUSG00000005566

NCBI accession no.

NM_011588

shipped in

ambient

storage temp.

−20°C

Gene Information

mouse ... TRIM28(21849) , Trim28(21849)

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

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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A Bakr et al.
Nucleic acids research, 43(6), 3154-3166 (2015-03-11)
Ataxia-telangiectasia mutated (ATM) is needed for the initiation of the double-strand break (DSB) repair by homologous recombination (HR). ATM triggers DSB end resection by stimulating the nucleolytic activity of CtIP and MRE11 to generate 3'-ssDNA overhangs, followed by RPA loading
Estela Cruvinel et al.
Human molecular genetics, 23(17), 4674-4685 (2014-04-25)
Prader-Willi syndrome (PWS), a disorder of genomic imprinting, is characterized by neonatal hypotonia, hypogonadism, small hands and feet, hyperphagia and obesity in adulthood. PWS results from the loss of paternal copies of the cluster of SNORD116 C/D box snoRNAs and

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