Nociceptin CRISPR/Cas9 KO Plasmid (m): sc-421945
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Nociceptin CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 Nociceptin 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nociceptin CRISPR/Cas9 KO Plasmid (m) | sc-421945 | 20 µg | $397.00 |
Overview
Pnoc encodes nociceptin/orphanin FQ, an endogenous neuropeptide ligand for the opioid receptor-like 1 receptor (OPRL1/NOP) that modulates neuronal excitability and synaptic transmission. Nociceptin signaling engages Gi/o-coupled pathways that reduce adenylyl cyclase activity, regulate cAMP/PKA outputs, and influence ion channel conductance and neurotransmitter release. In the central nervous system and peripheral tissues, this axis contributes to regulation of nociception, stress responsivity, reward circuitry, and neuroendocrine function. Dysregulation of PNOC–NOP signaling has been implicated in phenotypes relevant to pain processing, anxiety- and depression-like behaviors, substance use–related neuroadaptations, and inflammatory modulation.
Nociceptin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Pnoc gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Pnoc 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 Pnoc 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 Nociceptin protein expression.
This CRISPR knockout system enables efficient generation of Pnoc-deficient cell models for investigation of Nociceptin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Pnoc exon(s) critical for Nociceptin 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 Pnoc genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Nociceptin CRISPR/Cas9 KO Plasmid (m) and Nociceptin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Pnoc locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Nociceptin HDR Plasmid (m) and Nociceptin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Pnoc homology arms to support homology-directed repair at defined Pnoc 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.