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Merck

HSTUD0500

Sigma-Aldrich

MISSION® Synthetic microRNA Inhibitor, Human

hsa-miR-33b-5p

Synonym(e):

hsa-miR-33b

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About This Item

UNSPSC-Code:
12352200
NACRES:
NA.51

Produktlinie

MISSION®

Form

solid

Ausgereifte Sequenz

GUGCAUUGCUGUUGCAUUGC

Sanger-Hinterlegungsnummer ausgereifte/nicht ausgereifte Sequenzen

Sanger microRNA-Hinterlegungsnummer

Lagertemp.

−20°C

Allgemeine Beschreibung

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.

  • 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)

Sonstige Hinweise

Based on miRBase V19

Rechtliche Hinweise

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

Piktogramme

Health hazard

Signalwort

Warning

H-Sätze

Gefahreneinstufungen

STOT RE 2 Inhalation

Zielorgane

Respiratory Tract

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Lot/Batch Number

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Die Dokumentenbibliothek aufrufen

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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