LECT2 Double Nickase Plasmid (h): sc-407039-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LECT2 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
- LECT2 Double Nickase Plasmid (h) and LECT2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LECT2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LECT2 Antibody (B-6): sc-398071
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LECT2 Double Nickase Plasmid (h) | sc-407039-NIC | 20 µg | $410.00 |
Human LECT2 encodes leukocyte cell-derived chemotaxin 2, a secreted hepatokine and immunomodulatory protein implicated in leukocyte chemotaxis and regulation of inflammatory signaling. LECT2 is linked to hepatic metabolic and immune homeostasis and has been associated with pathways influencing cytokine responses, tissue remodeling, and extracellular milieu changes. Altered LECT2 expression has been reported across liver pathologies and systemic inflammatory states, and the protein is studied as a context-dependent modulator of tumor biology and fibrosis-related processes. These features make LECT2 a useful target for dissecting crosstalk between hepatocyte-derived factors, innate immune cell recruitment, and microenvironmental regulation.
LECT2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LECT2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LECT2. 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 LECT2 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 LECT2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.