IRS-3 CRISPR/Cas9 KO Plasmid (m): sc-421151
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRS-3 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 IRS-3 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRS-3 CRISPR/Cas9 KO Plasmid (m) | sc-421151 | 20 µg | $397.00 |
Overview
Irs3 encodes insulin receptor substrate 3 (IRS-3), a cytoplasmic adaptor that couples activated insulin and IGF-1 receptors to downstream signaling through PI3K–AKT and MAPK pathways. By providing phosphotyrosine docking sites for SH2-domain proteins, IRS-3 supports regulation of glucose uptake, glycogen synthesis, lipid metabolism, and growth-factor–dependent proliferation. In mouse models, altered IRS-family signaling is broadly relevant to insulin resistance, obesity-associated metabolic dysfunction, and inflammatory crosstalk that influences energy homeostasis. Studying IRS-3 helps dissect tissue-specific signaling bias and compensatory network behavior among IRS paralogs in metabolic and endocrine biology.
IRS-3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Irs3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Irs3 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 Irs3 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 IRS-3 protein expression.
This CRISPR knockout system enables efficient generation of Irs3-deficient cell models for investigation of IRS-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Irs3 exon(s) critical for IRS-3 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 Irs3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IRS-3 CRISPR/Cas9 KO Plasmid (m) and IRS-3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Irs3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IRS-3 HDR Plasmid (m) and IRS-3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Irs3 homology arms to support homology-directed repair at defined Irs3 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.