SCR7 |
| Catalog No.GC12106 |
SCR7 es una forma inestable que se puede autociclar en una forma estable de pirazina SCR7. La pirazina SCR7 es un inhibidor de la ADN ligasa IV que bloquea la uniÓn de extremos no homÓlogos (NHEJ) de una manera dependiente de la ligasa IV. La pirazina SCR7 también es un potenciador de CRISPR/Cas9 que aumenta la eficiencia de la reparaciÓn dirigida por homologÍa (HDR) mediada por Cas9. La pirazina SCR7 induce la apoptosis celular y tiene actividad anticancerÍgena.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1533426-72-0
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Scr7 is a DNA ligase IV inhibitor, initially identified as an anti-cancer agent [1].
Scr7 targets the DNA binding domain of DNA ligase IV, reducing its affinity for double strand breaks (DSBs) and inhibiting its function. Scr7 also inhibits DNA ligase III (but not DNA ligase I), albeit less efficiently. Cells were treated with doxycycline to induce Cas9 expression, with various concentrations of Scr7 for 24 h. Scr7 maintained cells capable of entering S/G2 phase, which is necessary for HDR. [1] Treatment of mice with Scr7 affects lymphocyte development, as DNA ligase IV plays a key role in the joining of coding ends during V(D)J recombination by means of C-NHEJ16. The defects in lymphocyte development upon Scr7 treatment are transient and reversible, due to the noncovalent mode of binding of Scr7. Scr7 enhanced the frequency of HDR by transiently blocking NHEJ (with the exception of DNA ligase I–dependent alt-NHEJ), resulting in precise genome editing by CRISPR-Cas9 in both cultured cells and in mice. [2]
References:
[1]. Srivastava M, Nambiar M, Sharma S et al. An inhibitor of nonhomologous end-joining abrogates double-strand break repair and impedes cancer progression. Cell. 2012 Dec 21;151(7):1474-87. doi: 10.1016/j.cell.2012.11.054.
[2]. Maruyama T, Dougan SK, Truttmann MC et al.Increasing the efficiency of precise genome editing with CRISPR-Cas9 by inhibition of nonhomologous end joining. Nat Biotechnol. 2015 Mar 23. doi: 10.1038/nbt.3190. [Epub ahead of print]
Average Rating: 5 (Based on Reviews and 9 reference(s) in Google Scholar.)
GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
Required fields are marked with *