CRBN Double Nickase Plasmid (h): sc-412142-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRBN 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
- CRBN Double Nickase Plasmid (h) and CRBN Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CRBN. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRBN Double Nickase Plasmid (h) | sc-412142-NIC | 20 µg | $410.00 | |||
CRBN Double Nickase Plasmid (h2) | sc-412142-NIC-2 | 20 µg | $410.00 |
CRBN (cereblon) encodes a substrate receptor of the CRL4^CRBN E3 ubiquitin ligase complex that couples CUL4A/DDB1 to specific target proteins for ubiquitination and proteasomal turnover. Through regulation of protein homeostasis, CRBN influences cell-cycle progression, differentiation programs, and stress-responsive signaling pathways. CRBN is also recognized for its role in small-molecule–dependent substrate recruitment, linking ubiquitin-mediated degradation to pharmacology-relevant biology. Altered CRBN expression or function has been associated with neurodevelopmental phenotypes and with changes in cellular sensitivity to proteostasis perturbation, supporting its relevance in mechanistic disease models.
CRBN Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CRBN locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CRBN. 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 CRBN 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 CRBN-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.