XAP8 Double Nickase Plasmid (h): sc-412247-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- XAP8 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
- XAP8 Double Nickase Plasmid (h) and XAP8 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RSF1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
XAP8 Double Nickase Plasmid (h) | sc-412247-NIC | 20 µg | $410.00 |
RSF1 encodes the human XAP8 protein, a chromatin-associated factor implicated in nucleosome remodeling and transcriptional regulation through interactions with ATP-dependent chromatin remodeling machinery. By modulating chromatin accessibility, RSF1 influences DNA replication timing, DNA damage responses, and cell-cycle progression, linking it to broader genome maintenance pathways. Altered RSF1 expression or copy number has been reported in multiple tumor contexts and is often studied for its contributions to proliferation, chromosomal instability, and stress-adaptive transcriptional programs. These characteristics make RSF1/XAP8 a useful target for dissecting epigenetic regulation mechanisms and their roles in disease-relevant cellular phenotypes.
XAP8 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RSF1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RSF1. 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 RSF1 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 RSF1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.