CNTFRα CRISPR/Cas9 KO Plasmid (h): sc-402322
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CNTFRα CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the CNTFRα genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- 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 CRISPR/Cas9 KO Plasmid (h) | sc-402322 | 20 µg | $397.00 |
Overview
CNTFR (ciliary neurotrophic factor receptor alpha; CNTFRα) encodes a glycosylphosphatidylinositol (GPI)-anchored receptor subunit that binds ciliary neurotrophic factor and assembles with LIFR and IL6ST/GP130 to initiate signaling. Receptor engagement activates JAK/STAT, MAPK/ERK, and PI3K/AKT pathways that regulate neuronal survival, differentiation, and glial responses, and can influence broader cytokine signaling cross-talk. CNTFRα contributes to neurodevelopmental and neuromuscular biology and is frequently studied in contexts of motor neuron maintenance, peripheral nerve injury responses, and neuroinflammatory signaling. Altered CNTF–CNTFR axis activity has been associated with neurological phenotypes and disease-relevant processes such as axon integrity, muscle innervation, and cell fate regulation.
CNTFRα CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CNTFR gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CNTFR together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the CNTFR open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish CNTFRα protein expression.
This CRISPR knockout system enables efficient generation of CNTFR-deficient cell models for investigation of CNTFRα signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CNTFR exon(s) critical for CNTFRα function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple CNTFR genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CNTFRα CRISPR/Cas9 KO Plasmid (h) and CNTFRα CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CNTFR locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CNTFRα HDR Plasmid (h) and CNTFRα HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CNTFR homology arms to support homology-directed repair at defined CNTFR target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.