Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CtIP Double Nickase Plasmid (h): sc-401292-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CtIP Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- CtIP Double Nickase Plasmid (h) and CtIP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RBBP8. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CtIP Antibody (D-4): sc-271339
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CtIP Double Nickase Plasmid (h) | sc-401292-NIC | 20 µg | $410.00 | |||
CtIP Double Nickase Plasmid (h2) | sc-401292-NIC-2 | 20 µg | $410.00 |
RBBP8 encodes CtIP, a conserved DNA end-resection factor that coordinates initiation of homologous recombination by promoting 5′–3′ processing of double-strand breaks and facilitating RAD51 loading. CtIP functions at the interface of DNA damage signaling and cell-cycle control, integrating with BRCA1- and MRN-dependent pathways to regulate checkpoint activation, replication fork stability, and repair pathway choice between homologous recombination and alternative end joining. Through its role in maintaining genome integrity, altered CtIP activity is linked to chromosomal instability and has been investigated in the context of cancer biology and tumor suppressor networks. CtIP-dependent resection also influences class switch recombination and other programmed DNA break processes, making RBBP8 a key node for studying repair fidelity and mutagenesis.
CtIP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RBBP8 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RBBP8. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt RBBP8 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of RBBP8-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.