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.
C3aR CRISPR/Cas9 KO Plasmid (m): sc-419392
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C3aR 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 C3aR 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: C3aR Antibody (D-12): sc-133172
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C3aR CRISPR/Cas9 KO Plasmid (m) | sc-419392 | 20 µg | $397.00 |
Overview
Mouse C3ar1 encodes the complement component 3a receptor (C3aR), a G protein-coupled receptor that binds the anaphylatoxin C3a generated during complement activation. C3aR signaling modulates leukocyte chemotaxis, degranulation, cytokine release, and vascular responses, integrating innate immune cues with downstream MAPK, PI3K/AKT, and calcium-dependent pathways. In myeloid cells, microglia, and other immune-responsive compartments, C3aR contributes to inflammation resolution as well as amplification depending on context. Dysregulated C3aR activity has been implicated in models of allergic airway inflammation, autoimmune pathology, infection-associated immunopathology, and neuroinflammatory processes.
C3aR CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the C3ar1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the C3ar1 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 C3ar1 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 C3aR protein expression.
This CRISPR knockout system enables efficient generation of C3ar1-deficient cell models for investigation of C3aR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting C3ar1 exon(s) critical for C3aR 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 C3ar1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by C3aR CRISPR/Cas9 KO Plasmid (m) and C3aR CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the C3ar1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by C3aR HDR Plasmid (m) and C3aR HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by C3ar1 homology arms to support homology-directed repair at defined C3ar1 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.