LIFR Double Nickase Plasmid (h): sc-400861-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LIFR 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
- LIFR Double Nickase Plasmid (h) and LIFR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LIFR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LIFR Antibody (A-10): sc-515337
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LIFR Double Nickase Plasmid (h) | sc-400861-NIC | 20 µg | $410.00 | |||
LIFR Double Nickase Plasmid (h2) | sc-400861-NIC-2 | 20 µg | $410.00 |
Leukemia inhibitory factor receptor (LIFR) is a type I cytokine receptor that partners with gp130 to mediate signaling by LIF and related IL-6 family cytokines. Ligand engagement promotes activation of JAK/STAT, MAPK/ERK, and PI3K/AKT pathways, coordinating transcriptional programs that regulate cell fate decisions including differentiation, survival, and tissue homeostasis. LIFR-dependent signaling is studied in developmental biology and stem cell contexts, and altered receptor function or expression has been associated with dysregulated growth control and inflammatory signaling in multiple disease settings. As a cell-surface receptor, LIFR also provides a tractable node for dissecting cytokine-receptor cross-talk and downstream pathway wiring.
LIFR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LIFR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LIFR. 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 LIFR 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 LIFR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.