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Merck
CN

EMU149771

MISSION® esiRNA

targeting mouse Myb

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NACRES:
NA.51
UNSPSC Code:
41105324

主要文件

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产品名称

MISSION® esiRNA, targeting mouse Myb

description

Powered by Eupheria Biotech

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

Quality Level

100

Gene Information

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

相关类别

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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分析证书(COA)

Lot/Batch Number
FVU
SRU
PMU
QCS
IET

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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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