ADAM22 CRISPR/Cas9 KO Plasmid (m): sc-418988
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADAM22 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 ADAM22 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: ADAM22 Antibody (C-2): sc-373931
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAM22 CRISPR/Cas9 KO Plasmid (m) | sc-418988 | 20 µg | $397.00 |
Overview
Adam22 encodes ADAM22, a catalytically inactive ADAM-family transmembrane protein enriched in the nervous system that functions as an adhesion/scaffolding component at synapses. ADAM22 forms complexes with LGI1 and postsynaptic receptors to regulate glutamatergic transmission, synapse maturation, and neuronal excitability, influencing dendritic spine organization and circuit stability. Through these interactions, ADAM22 impacts synaptic signaling pathways and activity-dependent plasticity that are central to neurodevelopment and network homeostasis. Dysregulation of the ADAM22–LGI1 axis has been linked to seizure susceptibility and neurodevelopmental phenotypes, making Adam22 a useful target for mechanistic studies of synaptic dysfunction in disease-relevant models.
ADAM22 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adam22 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adam22 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 Adam22 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 ADAM22 protein expression.
This CRISPR knockout system enables efficient generation of Adam22-deficient cell models for investigation of ADAM22 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adam22 exon(s) critical for ADAM22 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 Adam22 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADAM22 CRISPR/Cas9 KO Plasmid (m) and ADAM22 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adam22 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADAM22 HDR Plasmid (m) and ADAM22 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adam22 homology arms to support homology-directed repair at defined Adam22 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.