Molecular Weight(MW): 332.38
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.
Cited by 5 Publications
2 Customer Reviews
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
Cell Res, 2017, 27(6):801-814. SCR7 purchased from Selleck.
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.
J Cell Mol Med, 2017, 21(12):3337-3346. SCR7 purchased from Selleck.
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|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.|
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.
|In vitro||DMSO||66 mg/mL (198.56 mM)|
|Ethanol||3 mg/mL warmed (9.02 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.
* 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.
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Frequently Asked Questions
What should I do if I got precipitate out of solution after a freeze thaw and cannot re-suspend it?
Some compounds will precipitate out of solution after freeze/thaw, especially at very high concentration. You can warm it up to 45 degree and sonicate it to help it dissolve, of course, adding more DMSO will help too.