MO25 CRISPR/Cas9 KO Plasmid (m): sc-419399
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MO25 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 MO25 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: MO25 Antibody (919I2G): sc-517655
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MO25 CRISPR/Cas9 KO Plasmid (m) | sc-419399 | 20 µg | $397.00 |
Overview
Cab39 encodes the MO25 scaffolding protein, an essential binding partner for the LKB1 (STK11) kinase complex that stabilizes and allosterically enhances AMPK-related kinases. Through this role, MO25 contributes to energy-sensing signaling, cell polarity establishment, and stress-responsive control of metabolism via pathways linked to AMPK and related kinases such as MARK and SIK family members. In mouse cells, disruption of Cab39 can alter phosphorylation networks that influence cytoskeletal organization, epithelial polarity, and growth control programs coordinated by LKB1-dependent signaling. Because LKB1–AMPK axis dysregulation is broadly implicated in metabolic imbalance and tumor biology, Cab39 is frequently studied as a modulatory node affecting these processes in model systems.
MO25 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cab39 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cab39 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 Cab39 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 MO25 protein expression.
This CRISPR knockout system enables efficient generation of Cab39-deficient cell models for investigation of MO25 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cab39 exon(s) critical for MO25 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 Cab39 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MO25 CRISPR/Cas9 KO Plasmid (m) and MO25 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cab39 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MO25 HDR Plasmid (m) and MO25 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cab39 homology arms to support homology-directed repair at defined Cab39 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.