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EMU081361

Sigma-Aldrich

MISSION® esiRNA

targeting mouse Ralbp1

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About This Item

UNSPSC代码:
41105324
NACRES:
NA.51

描述

Powered by Eupheria Biotech

质量水平

产品线

MISSION®

形式

lyophilized powder

esiRNA cDNA靶序列

TTATGCCCCGATTTGAAGAGGCTTGTGGGAAGACCACAGAGATGGAGAAAGTGCAGGAATTCCAGCGCTTGCTCCGGGAACTGCCGGAGTGCAATCATCTTCTGCTTTCCTGGCTCATTGTGCACCTGGACCACGTCATTGCGAAGGAGCTGGAAACGAAGATGAACATCCAGAACATCTCTATAGTGCTGAGCCCCACCGTGCAGATCAGCAATCGGGTCCTGTACGTGCTTTTCACACATGTGCAAGAGCTCTTTGGCACCGTGGTCCTGAAGCAAGTAACAAGACCTCTGCGCTGGTCCAACATGGCCACGATGCCCACACTGCCAGAGACCCAAGCAGGCATCAAGGAGGAGATCAGGAGACAGGAGTTCCTTTTGAATTGTTTACATCGAGATCTGCAGGGCGGGATAAAGGACTTATCTAAAGAAGAAAGATTATGGGAAGTACAGAGGATTCTGACTGCCCTCAAG

基因组数据库 |小鼠登记号

NCBI登记号

运输

ambient

储存温度

−20°C

基因信息

相关类别

一般描述

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.

法律信息

MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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Yoshiko Kaku et al.
Cellular signalling, 27(9), 1713-1719 (2015-05-26)
The present study investigated 1,2-diarachidonoyl-sn-glycero-3-phosphoethanolamine (DAPE)-induced cell death in malignant pleural mesothelioma (MPM) cells. DAPE reduced cell viability in NCI-H28, NCI-H2052, NCI-H2452, and MSTO-211H MPM cell lines in a concentration (1-100μM)-dependent manner. In the flow cytometry using propidium iodide (PI)
W He et al.
Oncogene, 33(23), 3004-3013 (2013-07-09)
Killing cancer cells through the induction of apoptosis is one of the main mechanisms of chemotherapy. However, numerous cancer cells have primary or acquired apoptosis resistance, resulting in chemoresistance. In this study, using a novel chalcone derivative chalcone-24 (Chal-24), we
H Schoeneberger et al.
Oncogene, 34(31), 4032-4043 (2014-11-11)
Evasion of apoptosis in pediatric acute lymphoblastic leukemia (ALL) is linked to aberrant expression of inhibitor of apoptosis (IAP) proteins and dysregulated redox homeostasis, rendering leukemic cells vulnerable to redox-targeting therapies. Here we discover that inhibition of antioxidant defenses via

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