Z-NCTS

Z-NCTS potently stabilizes 11-mer UGG/UGG-containing dsRNA duplexes with a ΔT_m of 27.9 °C and binds in a 1:1 stoichiometry^[1].
Z-NCTS induces stable hairpin formation at the 5'UTR of lucG3 mRNA in a concentration-dependent manner, as detected by RTase stop assay^[1].
Z-NCTS dose-dependently suppresses translation from mRNAs (lucG3, GFPG3) containing its inducible hairpin sequence in the 5'UTR, without affecting translation from wild-type mRNAs (lucWT, GFPWT) in an E. coli cell-free system^[1].
Z-NCTS activates the RNA cleaving activity of engineered HHR1 by stabilizing its tertiary structure, even under low Mg²⁺ conditions, with activity increasing in a concentration-dependent manner^[1].
Z-NCTS induces folding of the unfolded HHR1-HHRS' complex into a compact, active tertiary structure, as evidenced by increased electrophoretic mobility matching native wild-type HHR-HHRS'^[1].
Z-NCTS dose-dependently suppresses firefly luciferase expression in HeLa cells by activating HHR1 ribozyme cleavage of mRNA, reducing expression by 65% (HHR1-st1) and 75% (HHR1-st3) at 0.6 μM^[1].
Z-NCTS strongly stabilizes the secondary structure of mismatch-containing designer model RNAs, with the greatest stabilization (ΔTm of 38.1°C) observed for the stem-loop 3-derived R-SL3-S2 variant at 30 μM, while showing weaker, potentially non-specific stabilization of wild-type model RNAs^[2].
Z-NCTS (40-80 μM; 30 min) inhibits Cas9-mediated DNA cleavage in vitro when paired with designer sgRNAs containing mismatch-based MBL-binding sites, but exhibits non-specific activity against wild-type sgRNAs at concentrations above 40 μM^[2].
Z-NCTS (40-80 μM; 30 min) inhibits Cas9-mediated DNA cleavage in vitro when paired with designer tracrRNAs containing mismatch-based MBL-binding sites, but exhibits non-specific activity against wild-type tracrRNAs^[2].
Z-NCTS (11.4 μM) weakly stabilizes the r(CGG)/r(CGG) 11-mer RNA duplex (ΔT_m = +2.1 °C) and strongly stabilizes the r(UGG)/r(UGG) 11-mer RNA duplex (ΔT_m = +27.9 °C)^[3].
Z-NCTS (40 μM) binds to r(UGG)/r(UGG) and r(AGG)/r(AGG) 26-mer hairpin RNAs with 1:1 stoichiometry, and to r(GGG)/r(GGG) 26-mer hairpin RNA with 2:1 stoichiometry^[3].
Z-NCTS binds to r(UGG)/r(UGG) RNA with submicromolar affinity (K_d = 0.3 μM via CD, 0.27 μM via ITC) and to r(AGG)/r(AGG) RNA with a K_d of 2 mM via CD titration^[3].
Z-NCTS (5-15 μM) dose-dependently inhibits translation of lucG3 mRNA (50% inhibition at 5 μM) and lucG2 mRNA (15% inhibition at 5 μM) in a reconstituted E. coli cell-free translation system, while having minimal effect on lucWT mRNA translation^[3].
Z-NCTS (1-10 μM) induces stable hairpin structures in the 5'-UTRs of lucG2 and lucG3 mRNAs, with a more pronounced effect on lucG3, while having no such effect on lucWT mRNA^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.