SR-A CRISPR/Cas9 KO Plasmid (m2): sc-422832-KO-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SR-A CRISPR/Cas9 Knockout (KO) Plasmid (m2) 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 SR-A 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: SR-A Antibody (B-9): sc-166139
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SR-A CRISPR/Cas9 KO Plasmid (m2) | sc-422832-KO-2 | 20 µg | $397.00 |
Overview
Msr1 encodes scavenger receptor class A (SR-A), a macrophage-enriched pattern-recognition receptor that binds modified lipoproteins, apoptotic cells, and microbial ligands to coordinate uptake and innate immune signaling. SR-A drives receptor-mediated endocytosis and phagocytosis, shaping lipid handling, inflammatory responses, and resolution of tissue damage through crosstalk with Toll-like receptor pathways and cytokine networks. In mouse models, altered Msr1/SR-A activity has been linked to dysregulated foam cell formation, sterile inflammation, and susceptibility to infection, making it relevant to studies of atherosclerosis-like processes, neuroinflammation, and metabolic disease mechanisms. Its expression in myeloid lineages also supports research into macrophage polarization, antigen processing, and clearance pathways in complex tissue microenvironments.
SR-A CRISPR/Cas9 KO Plasmid (m2) is a pool of plasmids designed for targeted disruption of the Msr1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Msr1 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 Msr1 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 SR-A protein expression.
This CRISPR knockout system enables efficient generation of Msr1-deficient cell models for investigation of SR-A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Msr1 exon(s) critical for SR-A 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 Msr1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SR-A CRISPR/Cas9 KO Plasmid (m) and SR-A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Msr1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SR-A HDR Plasmid (m) and SR-A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Msr1 homology arms to support homology-directed repair at defined Msr1 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.