Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CNTFRα Double Nickase Plasmid (h): sc-402322-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CNTFRα 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
- CNTFRα Double Nickase Plasmid (h) and CNTFRα Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CNTFR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CNTFRα Antibody (AN-B2): sc-9993
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CNTFRα Double Nickase Plasmid (h) | sc-402322-NIC | 20 µg | $410.00 | |||
CNTFRα Double Nickase Plasmid (h2) | sc-402322-NIC-2 | 20 µg | $410.00 |
Ciliary neurotrophic factor receptor alpha (CNTFRα), encoded by CNTFR, is a glycosylphosphatidylinositol (GPI)-anchored receptor subunit that confers ligand binding specificity within the CNTF receptor complex. Upon CNTF engagement, CNTFRα cooperates with LIFR and gp130 to initiate JAK/STAT signaling, with additional coupling to MAPK/ERK and PI3K/AKT pathways that regulate neuronal survival, differentiation, and glial biology. CNTFR pathway activity is widely studied in the context of neurodevelopment and neurodegeneration, where altered receptor expression or signaling tone can influence neuronal maintenance and response to injury. Dysregulation of CNTF/CNTFR-axis signaling has been linked to disease-relevant cellular phenotypes in models of motor neuron and retinal disorders, supporting mechanistic investigation in human cell systems.
CNTFRα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CNTFR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CNTFR. 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 CNTFR 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 CNTFR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.