Mena CRISPR/Cas9 KO Plasmid (m): sc-420173
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mena 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 Mena 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: Mena Antibody (21): sc-135988
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mena CRISPR/Cas9 KO Plasmid (m) | sc-420173 | 20 µg | $397.00 |
Overview
Enah encodes Mena (mammalian enabled), an Ena/VASP family actin regulatory protein that promotes filament elongation and coordinates actin–membrane coupling at lamellipodia, filopodia, and adhesion sites. Mena integrates signaling from Rho-family GTPases, integrin-mediated focal adhesion pathways, and growth factor inputs to shape cell polarity, migration, and tissue morphogenesis. In mouse systems, Enah activity is commonly examined in contexts such as neural development, epithelial remodeling, and cytoskeletal dynamics underlying invasive cell behavior. Dysregulated Ena/VASP-dependent actin remodeling is broadly linked to altered cell motility programs relevant to cancer biology and neurodevelopmental phenotypes in experimental models.
Mena CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Enah gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Enah 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 Enah 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 Mena protein expression.
This CRISPR knockout system enables efficient generation of Enah-deficient cell models for investigation of Mena signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Enah exon(s) critical for Mena 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 Enah genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Mena CRISPR/Cas9 KO Plasmid (m) and Mena CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Enah locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Mena HDR Plasmid (m) and Mena HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Enah homology arms to support homology-directed repair at defined Enah 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.