α2C-AR CRISPR/Cas9 KO Plasmid (m): sc-419025
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α2C-AR 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 α2C-AR 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 | |
α2C-AR CRISPR/Cas9 KO Plasmid (m) | sc-419025 | 20 µg | $397.00 |
Overview
Adra2c encodes the mouse α2C-AR, an inhibitory G protein–coupled receptor for catecholamines that primarily couples to Gi/Go to suppress adenylyl cyclase activity, reduce cAMP/PKA signaling, and modulate ion channel function. Through regulation of presynaptic neurotransmitter release and sympathetic outflow, α2C-AR influences synaptic transmission, vascular tone, and stress-responsive neuroendocrine signaling. Receptor activation can also engage βγ-dependent pathways that affect MAPK/ERK signaling and cellular excitability. Dysregulated adrenergic signaling involving ADRA2C has been associated with neuropsychiatric phenotypes and cardiovascular processes, making this gene relevant to studies of autonomic regulation and neural circuit function.
α2C-AR CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adra2c gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adra2c 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 Adra2c 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 α2C-AR protein expression.
This CRISPR knockout system enables efficient generation of Adra2c-deficient cell models for investigation of α2C-AR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adra2c exon(s) critical for α2C-AR 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 Adra2c genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by α2C-AR CRISPR/Cas9 KO Plasmid (m) and α2C-AR CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adra2c locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by α2C-AR HDR Plasmid (m) and α2C-AR HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adra2c homology arms to support homology-directed repair at defined Adra2c 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.