CRABP-I Double Nickase Plasmid (h2): sc-405485-NIC-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRABP-I Double Nickase Plasmid (h2) 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
- CRABP-I Double Nickase Plasmid (h2) and CRABP-I Double Nickase Plasmid (h22) encode distinct paired gRNA designs targeting CRABP1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRABP-I Double Nickase Plasmid (h2) | sc-405485-NIC-2 | 20 µg | $410.00 |
Human CRABP1 encodes cellular retinoic acid-binding protein 1 (CRABP-I), a high-affinity cytosolic carrier that sequesters and traffics all-trans retinoic acid, shaping its intracellular availability and spatiotemporal signaling. By modulating retinoid distribution, CRABP-I influences retinoic acid–dependent transcriptional programs mediated by nuclear receptors (RAR/RXR) and impacts processes including differentiation, proliferation, and developmental patterning. Altered retinoid homeostasis and CRABP1 expression have been associated with dysregulated signaling in cancer and other disorders linked to vitamin A metabolism and cellular differentiation states. CRABP1 gene editing and perturbation studies support mechanistic dissection of retinoid signaling networks, ligand buffering dynamics, and transcriptional outcomes in relevant human cell models.
CRABP-I Double Nickase Plasmid (h2) consists of a matched pair of plasmids engineered for high-specificity editing of the CRABP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CRABP1. 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 CRABP1 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 CRABP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.