Epiregulin CRISPR/Cas9 KO Plasmid (m): sc-420224
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Epiregulin 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 Epiregulin 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: Epiregulin Antibody (C-9): sc-376284
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Epiregulin CRISPR/Cas9 KO Plasmid (m) | sc-420224 | 20 µg | $397.00 |
Overview
Mouse Ereg encodes epiregulin, a secreted member of the EGF family that engages EGFR/ERBB receptors to modulate paracrine and autocrine signaling. Epiregulin regulates epithelial and stromal cell proliferation, survival, and migration, integrating with MAPK/ERK and PI3K/AKT pathway activity and shaping wound repair and tissue remodeling programs. Ereg expression is responsive to inflammatory and injury cues and is frequently studied in contexts where EGFR-network signaling intersects with cytokine-driven microenvironments. Dysregulated epiregulin signaling has been linked to altered barrier function, fibrotic remodeling, and oncogenic signaling circuits, supporting its use as a mechanistic node in studies of tumor–stroma interactions and inflammation-associated growth factor signaling.
Epiregulin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ereg gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ereg 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 Ereg 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 Epiregulin protein expression.
This CRISPR knockout system enables efficient generation of Ereg-deficient cell models for investigation of Epiregulin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ereg exon(s) critical for Epiregulin 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 Ereg genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Epiregulin CRISPR/Cas9 KO Plasmid (m) and Epiregulin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ereg locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Epiregulin HDR Plasmid (m) and Epiregulin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ereg homology arms to support homology-directed repair at defined Ereg 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.