產品線
MISSION®
形狀
solid
成熟序列
GUGCAUUGCUGUUGCAUUGC
Sanger 成體/幼體登錄號
Sanger microRNA登錄號
儲存溫度
−20°C
一般說明
Individual synthetic microRNA inhibitors were designed using a proprietary algorithm, which is based on the work of Haraguchi, T, et al. and in collaboration with Dr. Hideo Iba, University of Tokyo. This algorithm utilizes the tough decoy (TuD) design. miRNA are known to regulate gene expression in a variety of manners, including translational repression, mRNA cleavage and deadenylation.
The MISSION synthetic miRNA Inhibitors are small, double-stranded RNA molecules designed to inhibit a specific mature miRNA. The miRNA inhibitors were designed using the mature miRNA sequence information from miRBase and are 2′-O-methylated RNA duplexes with a miRNA binding site on each strand. Optimal miRNA inhibition is provided after transfection due to the robust secondary structure of the inhibitor.
Two negative controls are available: Arabidopsis thaliana sequence (NCSTUD001) and Caenorhabditis elegans sequence (NCSTUD002)
The MISSION synthetic miRNA Inhibitors are small, double-stranded RNA molecules designed to inhibit a specific mature miRNA. The miRNA inhibitors were designed using the mature miRNA sequence information from miRBase and are 2′-O-methylated RNA duplexes with a miRNA binding site on each strand. Optimal miRNA inhibition is provided after transfection due to the robust secondary structure of the inhibitor.
- Long lasting inhibition at very low dosage
- Excellent resistance to cellular nucleases
- Custom synthesis available for a variety of species
Two negative controls are available: Arabidopsis thaliana sequence (NCSTUD001) and Caenorhabditis elegans sequence (NCSTUD002)
其他說明
Based on miRBase V19
法律資訊
MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany
訊號詞
Warning
危險聲明
危險分類
STOT RE 2 Inhalation
標靶器官
Respiratory Tract
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
分析證明 (COA)
輸入產品批次/批號來搜索 分析證明 (COA)。在產品’s標籤上找到批次和批號，寫有 ‘Lot’或‘Batch’.。
Xiuxing Wang et al.
Cancer research, 77(18), 4947-4960 (2017-07-22)
Metabolic dysregulation drives tumor initiation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic alterations in glioblastomas with wild-type IDH are poorly understood. MYC promotes metabolic reprogramming in cancer, but targeting MYC has proven notoriously challenging. Here
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