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.
aggrecan CRISPR/Cas9 KO Plasmid (m): sc-419039
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- aggrecan 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 aggrecan 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 | |
aggrecan CRISPR/Cas9 KO Plasmid (m) | sc-419039 | 20 µg | $397.00 |
Overview
Acan encodes aggrecan, a major chondroitin sulfate proteoglycan of the cartilage extracellular matrix that provides compressive resilience by forming large aggregates with hyaluronan and link proteins. Aggrecan synthesis, secretion, and matrix assembly are central to chondrocyte differentiation and growth plate maturation, integrating with cartilage homeostasis programs influenced by TGF-β, BMP, and inflammatory cytokine signaling. Proteolytic cleavage of aggrecan by ADAMTS aggrecanases and matrix metalloproteinases contributes to extracellular matrix remodeling and loss of cartilage integrity. Dysregulated aggrecan turnover and reduced Acan expression are implicated in skeletal dysplasia phenotypes and degenerative joint processes, making Acan a core target for musculoskeletal and cartilage biology research in mouse models.
aggrecan CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Acan gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Acan 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 Acan 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 aggrecan protein expression.
This CRISPR knockout system enables efficient generation of Acan-deficient cell models for investigation of aggrecan signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Acan exon(s) critical for aggrecan 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 Acan genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by aggrecan CRISPR/Cas9 KO Plasmid (m) and aggrecan CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Acan locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by aggrecan HDR Plasmid (m) and aggrecan HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Acan homology arms to support homology-directed repair at defined Acan 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.