ADAM12 CRISPR/Cas9 KO Plasmid (m): sc-418983
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADAM12 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 ADAM12 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: ADAM12 Antibody (1G3): sc-293225
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAM12 CRISPR/Cas9 KO Plasmid (m) | sc-418983 | 20 µg | $397.00 |
Overview
ADAM12 (a disintegrin and metalloproteinase 12) is a membrane-anchored protease and adhesion regulator that modulates extracellular matrix remodeling, growth factor signaling, and cell–cell interactions. In mouse tissues, ADAM12 contributes to proteolytic shedding of cell-surface proteins and influences pathways linked to myogenesis, fibrosis, and stromal remodeling, including EGFR and TGF-β–associated processes. Its activity affects cell migration, differentiation, and mechanotransduction by altering ECM composition and receptor availability. Dysregulated ADAM12 expression or activity has been associated with pathological tissue remodeling and inflammation-related phenotypes, making it relevant for studying disease mechanisms in musculoskeletal and fibrotic contexts.
ADAM12 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adam12 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adam12 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 Adam12 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 ADAM12 protein expression.
This CRISPR knockout system enables efficient generation of Adam12-deficient cell models for investigation of ADAM12 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adam12 exon(s) critical for ADAM12 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 Adam12 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADAM12 CRISPR/Cas9 KO Plasmid (m) and ADAM12 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adam12 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADAM12 HDR Plasmid (m) and ADAM12 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adam12 homology arms to support homology-directed repair at defined Adam12 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.