ERM CRISPR/Cas9 KO Plasmid (m): sc-430518
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERM 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 ERM 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: ERM Antibody (H-06): sc-100941
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERM CRISPR/Cas9 KO Plasmid (m) | sc-430518 | 20 µg | $397.00 |
Overview
Etv5 encodes the ETS family transcription factor ERM, a sequence-specific regulator of gene expression that integrates signals from MAPK/ERK and receptor tyrosine kinase pathways to control proliferation, differentiation, and cell fate decisions. In mouse development, ERM contributes to organogenesis and tissue homeostasis by modulating transcriptional programs linked to stem/progenitor maintenance and lineage commitment. Etv5 activity has been connected to pathways governing Sertoli cell function, neuronal and epithelial differentiation, and adaptive responses to growth factor stimulation. Dysregulated ETS factor signaling, including altered ETV5/ERM-dependent transcriptional networks, is frequently studied in models of tumorigenesis, invasion, and resistance phenotypes without implying clinical outcomes.
ERM CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Etv5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Etv5 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 Etv5 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 ERM protein expression.
This CRISPR knockout system enables efficient generation of Etv5-deficient cell models for investigation of ERM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Etv5 exon(s) critical for ERM 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 Etv5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ERM CRISPR/Cas9 KO Plasmid (m) and ERM CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Etv5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ERM HDR Plasmid (m) and ERM HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Etv5 homology arms to support homology-directed repair at defined Etv5 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.