CR1L Double Nickase Plasmid (h): sc-405453-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CR1L 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
- CR1L Double Nickase Plasmid (h) and CR1L Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CR1L. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CR1L Double Nickase Plasmid (h) | sc-405453-NIC | 20 µg | $410.00 | |||
CR1L Double Nickase Plasmid (h2) | sc-405453-NIC-2 | 20 µg | $410.00 |
Complement receptor 1 like (CR1L) is a human gene annotated as a complement receptor–related member of the regulators of complement activation family, sharing structural features with CR1 that participate in opsonization and immune complex handling. By analogy to CR1, CR1L is relevant to processes linked to complement cascade control, innate immune surveillance, and crosstalk between complement signaling and cellular responses such as phagocytosis and inflammatory modulation. Variation in complement regulatory networks is broadly associated with immune dysregulation and inflammatory tissue damage, making CR1L a useful locus for mechanistic studies of complement-associated phenotypes. Experimental interrogation of CR1L supports research into complement-driven pathways, receptor-like domain function, and genotype–phenotype relationships in immune-relevant cellular models.
CR1L Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CR1L locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CR1L. 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 CR1L 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 CR1L-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.