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EMU149771

Sigma-Aldrich

MISSION® esiRNA

targeting mouse Myb

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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

AAATTTACACAAAGAAATATCCCAGTATTCCATGTATCTCAGTCACTAAACATACACAGAGAGATTTTTAAAAACCAGGAGAAGCATTATTTTGAATGTTAGCTAAATCCCAAGTAATACTTAATGCAACCCTCTAGGAGCTCATTTGTGGCTAATAATCTTGGAAATATCTTTATTATACTAAACCATTTCATGAGGAGAATTTTGTTGTCAGCTTGCTTGAAAAGTTATTACTGTATGAAATAGTTTTATTGAAAAAATTATATTTTTATTCAGTAATTTAATTTTGTAAATGCCAAATGGAGAAATGTGTTCGCTGCTATGGTTTTAGCCTGTAGTCATGCTGCTAGCTAGTGTCAGGGGGCAATAGAGCTTAGATGGAAAAAAGAGAAAGAGACTCGGTGTTAGATAACGGACTATGCACTAGTATTCCAGACTTTTTTATTTTTATATATATGTACCTTTTCCTTTTGTAATTGGAAAACTTATTTGGGAGAATTTTGCATTTGT

Ensembl | mouse accession no.

ENSMUSG00000019982

NCBI accession no.

NM_010848

shipped in

ambient

storage temp.

−20°C

Gene Information

mouse ... MYB(17863) , Myb(17863)

Related Categories

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

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P Basova et al.
Oncogene, 33(39), 4735-4745 (2013-10-15)
PU.1 downregulation within hematopoietic stem and progenitor cells (HSPCs) is the primary mechanism for the development of acute myeloid leukemia (AML) in mice with homozygous deletion of the upstream regulatory element (URE) of PU.1 gene. p53 is a well-known tumor
Likun Li et al.
Science signaling, 7(326), ra47-ra47 (2014-05-23)
Androgen deprivation is the standard treatment for advanced prostate cancer (PCa), but most patients ultimately develop resistance and tumor recurrence. We found that MYB is transcriptionally activated by androgen deprivation therapy or genetic silencing of the androgen receptor (AR). MYB

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