MIR96-IN-1 |
Catalog No.GC32929 |
MIR96-IN-1 targets the Drosha site in the miR-96 (miRNA-96, microRNA-96) hairpin precursor, inhibiting its biogenesis, derepressing downstream targets, and triggering apoptosis in breast cancer cells. MIR96-IN-1 binds to RNAs with Kds of 1.3, 9.4, 3.4, 1.3 and 7.4 μM for RNA1, RNA2, RNA3, RNA4 and RNA5, respectively.
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Cas No.: 1311982-88-3
Sample solution is provided at 25 µL, 10mM.
MIR96-IN-1 selectively inhibits biogenesis of microRNA-96, upregulating a protein target (FOXO1) and inducing apoptosis in cancer cells.Target: microRNA-96in vitro: MIR96-IN-1 inhibits biogenesis of its target precursor miRNA to varying extents : MIR96-IN-1 reduces the expression level of miR-96 by 90% at 40 μM. MIR96-IN-1 efficiently and selectively silences production of miR-96 at 40 μM while not affecting miR-182 or -183. Moreover, MIR96-IN-1 inhibits Drosha cleavage of pri-miR-96, as evidenced by an increase in the levels of pri-miR-96 and a reduction in levels of pre- and mature miR-96 in treated cells, as expected if MIR96-IN-1 binds to the Drosha site. [1]
[1]. Velagapudi SP, et al. Sequence-based design of bioactive small molecules that target precursor microRNAs. Nat Chem Biol. 2014 Apr;10(4):291-7. [2]. Haga CL, et al. Small Molecule Inhibition of miR-544 Biogenesis Disrupts Adaptive Responses to Hypoxia by Modulating ATM-mTOR Signaling. ACS Chem Biol. 2015 Oct 16;10(10):2267-76. [3]. Velagapudi SP, et al. Defining the RNA internal loops preferred by benzimidazole derivatives via 2D combinatorial screening and computational analysis. J Am Chem Soc. 2011 Jul 6;133(26):10111-8.
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