CD5L Double Nickase Plasmid (h): sc-404865-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD5L 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
- CD5L Double Nickase Plasmid (h) and CD5L Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CD5L. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD5L Antibody (F-1): sc-514283
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD5L Double Nickase Plasmid (h) | sc-404865-NIC | 20 µg | $410.00 | |||
CD5L Double Nickase Plasmid (h2) | sc-404865-NIC-2 | 20 µg | $410.00 |
CD5L (CD5 molecule-like), also known as AIM, encodes a secreted scavenger receptor cysteine-rich protein predominantly produced by macrophages and other myeloid cells. CD5L binds lipids and microbial components to modulate innate immune homeostasis, influencing macrophage survival, efferocytosis, and inflammatory polarization. It is implicated in pathways governing lipid metabolism and immune regulation, including responses that shape tissue inflammation and metabolic stress. Altered CD5L expression has been associated with inflammatory and metabolic disorders as well as tumor-associated macrophage biology, making it a useful target for mechanistic studies in immunometabolism and microenvironment research.
CD5L Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CD5L locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CD5L. 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 CD5L 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 CD5L-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.