|Solubility (25°C) *||In vitro||DMSO||66 mg/mL (198.56 mM)|
|Ethanol||3 mg/mL warmed (9.02 mM)|
|In vivo||2% DMSO+30% PEG 300+5% Tween 80+ddH2O||5mg/mL|
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
|Description||SCR7 is a specific DNA Ligase IV inhibitor, which blocks nonhomologous end-joining (NHEJ). It increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos.|
|In vitro||SCR7 effectively inhibits the formation of multimers at 200 μM and above. SCR7 successfully inhibits cell proliferation of MCF7, A549, HeLa, T47D, A2780, HT1080, and Nalm6 with IC50 of 40, 34, 44, 8.5, 120, 10, and 50 μM, respectively. SCR7 suppresses the NHEJ repair of CRISPR-Cas9-induced DSBs.SCR7 increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos.|
|In vivo||SCR7 treatment (10 mg/kg, i.m.) signiﬁcantly reduces breast adenocarcinoma-induced tumor, and exhibits 4-fold increase in lifespan compared with control group. However, in Swiss albino mice with Dalton’s lymphoma tumor model, SCR7 (20 mg/kg, i.p.) exhibits neither tumor regression nor increase in lifespan. In BALB/c mice, SCR7 (20 mg/kg, i.p.) signiﬁcantly enhances the cytotoxic effects of radiation, etoposide and 3-Aminobenzamide on tumor derived from Dalton’s lymphoma (DLA) cells.|
|Complementation of SCR7 Inhibition with Puriﬁed Ligase IV||Complementation experiment is carried out by adding increasing concentrations of puriﬁed Ligase IV/XRCC4 complex (30, 60, and 120 fmol) along with the oligomeric DNA substrates (5’ compatible and 5’-5’ noncompatible ends) to the SCR7-treatedextracts. Reactions are incubated for 2 h at 25℃. The reaction products are then resolved on 8% denaturing PAGE. The gel is dried and exposed and the signal is detected with a PhosphorImager and analyzed with Multi Gauge (V3.0) software.|
|Cell lines||MCF7, CEM, HeLa, A549, HT1080, A2780, T47D, Nalm6, N114 and K562 cells|
|Incubation Time||48 h|
Cell proliferation of cancer cells are determined by MTT and trypan blue assays. Briefly, MCF7, CEM, HeLa, A549, HT1080, A2780, T47D, Nalm6, N114 and K562 cells are grown in presence of SCR7 (10, 50, 100, and 250 μM) for 24 or 48 h, and subjected to MTT or trypan blue assays. Each experiment is repeated a minimum of three independent times.
|Animal Models||BALB/c mice|
Data from [Data independently produced by , , Cell Res, 2017, 27(6):801-814]
Knock-in efficiencies of mCherry knock-in at Actb locus by four strategies in mouse ES cells (A) were measured by FACS and compared with the group treated with NHEJ inhibitor (Scr7 or Nu7026), HR inhibitor (caffeine) or both. Results were presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, unpaired Student’s t-test
, , J Cell Mol Med, 2017, 21(12):3337-3346
The start codon CUG of PTEN-long was mutated to AUG and PTENlong expression is significantly increased. gRNA1 and gRNA2 have similar efficiency in driving PTEN-long expression (lanes 1 and 2). Combined gRNA1 and gRNA2 (lane 3) did not enhance PTEN-long expression compared to lane 1 and 2. The ssODN is required for mutation of CTG to ATG through HDR and without which PTEN-long is not expressed (lane 4). PTEN-long cDNA cloned into pcDNA3.1 with CTG to ATG mutation was highly expressed in transfected HEK293T cells (lane 5). Lane 6 is protein ladder. Lanes 7–10 indicate that the combination of gRNA and ssODN is required to facilitate HDR occurrence and double-strand DNA break.
Torsional stress promotes trinucleotidic expansion in spermatids. [Simard O, et al. Mutat Res, 2017, 800-802:1-7]PubMed: 28412438
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