1. Cell Cycle/DNA Damage
  2. CRISPR/Cas9

CRISPR/Cas9

CRISPR/Cas9 (Clustered Regularly-Interspaced Short Palindromic Repeats/Cas9) is a bacterial immune system that has been adapted for genome editing in mammalian cells. Cas9 is a programmable nuclease that generates double-stranded breaks (DSB) in DNA dictated by binding of a ~20 nucleotide recombinant “guide RNA” (gRNA) to the target site. DSB’s produced by Cas9 are most often repaired through the cell’s error-prone non-homologous end joining (NHEJ) pathway, resulting in small insertions or deletions (indels). The vast majority of indels shift the reading frame, introducing a premature stop codon or resulting in nonsense mediated decay of the mRNA-effectively “knocking out” a gene.

The CRISPR/Cas9 system has substantially advanced efforts in specific gene editing and has been successfully applied to modify the episomal genomes of human and other organisms. The CRISPR/Cas9 system utilizes a prokaryotic RNA-guided programmable nuclease that can make a double-strand DNA break (DSB) at a specific site under the guidance of a leading RNA. This DSB process depends on the co-expression of two basic components: a guide RNA (gRNA) and Cas9 nuclease. Making a specific DSB can trigger DNA repair via either error-prone non-homologous end joining (NHEJ) or homology-directed repair (HDR). In the presence of the CRISPR/Cas9 system, the NHEJ inhibitor SCR7 is proven to increase the efficiency of Cas9-mediated HDR by at least by 7-fold in mammalian cells. Genome editing via CRISPR/Cas9 has become an efficient and reliable way to make precise, targeted changes to the genome of living cells.

CRISPR/Cas9 Related Products (6):

Cat. No. Product Name Effect Purity
  • HY-12742
    SCR7 Agonist
    SCR7 is a DNA Ligase IV inhibitor, blocks nonhomologous end-joining (NHEJ). SCR7 increases CRISPR/Cas9-mediated editing frequency.
  • HY-16592
    Brefeldin A Activator
    Brefeldin A is a fungal metabolite that induces the Golgi proteins to redistribute into the ER, blocks the secretion from the Golgi apparatus and increases CRISPR/Cas9-mediated editing frequencies.
  • HY-13520
    Nocodazole Activator
    Nocodazole is a rapidly-reversible inhibitor of microtubule polymerization, which exhibits good potency against ABL, ABL(E255K), and ABL(T315I) with IC50 values of 0.21 μM, 0.53 μM, and 0.64 μM, respectively, and increases CRISPR/Cas9-mediated editing frequencies.
  • HY-11006
    KU-57788 Activator
    KU-57788 is a potent and selective inhibitor of DNA-PK, a modest inhibitor of BRD4 and BRDT, with IC50s of 13 nM, 1 μM and 3.5 μM, respectively, and also increases CRISPR/Cas9-mediated editing frequencies.
  • HY-16950
    4-Hydroxytamoxifen Agonist
    4-hydroxytamoxifen (OHT), an active metabolite of tamoxifen, is a selective estrogen receptor modulator, which increases CRISPR/Cas9-mediated editing frequency.
  • HY-19793
    RS-1 Activator
    RS-1 is a RAD51-stimulatory compound, which increases the DNA binding activity of RAD51.