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描述
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质量水平
产品线
MISSION®
表单
lyophilized powder
esiRNA cDNA靶序列
TTCATGGCTGAAATGTTGGAAACTGCTTCTATCCTCAGGTCTGCAACCAAAGATTCATTAATAATCATAGATGAATTGGGAAGAGGAACTTCTACCTACGATGGATTTGGGTTAGCATGGGCTATATCAGAATACATTGCAACAAAGATTGGTGCTTTTTGCATGTTTGCAACCCATTTTCATGAACTTACTGCCTTGGCCAATCAGATACCAACTGTTAATAATCTACATGTCACAGCACTCACCACTGAAGAGACCTTAACTATGCTTTATCAGGTGAAGAAAGGTGTCTGTGATCAAAGTTTTGGGATTCATGTTGCAGAGCTTGCTAATTTCCCTAAGCATGTAATAGAGTGTGCTAAACAGAAAGCCCTGGAACTTGAGGAGTTTCAGTATATTGGAGAATCGCAAGGATATGATATCATGGAACCAGCAGCAAAGAAGTGCTATCTGGAAAGAGAGCAAGGTGAAAAAATTATTCAGGAGTTCCTGTCCAAGGTGAAACAAATGCCCT
基因组数据库 |人类登记号
NCBI登记号
运输
ambient
储存温度
−20°C
基因信息
human ... MSH2(4436) , MSH2(4436)
一般描述
MISSION® shRNA是核糖核酸内切酶制备的siRNA。它们是靶向相同mRNA序列的siRNA异质混合物。这些多重沉默触发（multiple silencing trigger）导致高度特异性的、有效的基因沉默。
如需其他详细信息并查看所有可用的esiRNA选项，请访问SigmaAldrich.com/esiRNA。
如需其他详细信息并查看所有可用的esiRNA选项，请访问SigmaAldrich.com/esiRNA。
法律信息
MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany
储存分类代码
10 - Combustible liquids
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
Jennifer A McKinney et al.
Nature communications, 11(1), 236-236 (2020-01-15)
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Alaina R Martinez et al.
Genes, chromosomes & cancer, 56(8), 617-631 (2017-04-12)
Cancer cells require telomere maintenance to enable uncontrolled growth. Most often telomerase is activated, although a subset of human cancers are telomerase-negative and depend on recombination-based mechanisms known as ALT (Alternative Lengthening of Telomeres). ALT depends on proteins that are
Min Peng et al.
The EMBO journal, 33(15), 1698-1712 (2014-06-27)
Several proteins in the BRCA-Fanconi anemia (FA) pathway, such as FANCJ, BRCA1, and FANCD2, interact with mismatch repair (MMR) pathway factors, but the significance of this link remains unknown. Unlike the BRCA-FA pathway, the MMR pathway is not essential for
Daniel J McGrail et al.
Cancer cell, 37(3), 371-386 (2020-02-29)
Deficient DNA mismatch repair (dMMR) induces a hypermutator phenotype that can lead to tumorigenesis; however, the functional impact of the high mutation burden resulting from this phenotype remains poorly explored. Here, we demonstrate that dMMR-induced destabilizing mutations lead to proteome
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