SIMPL CRISPR/Cas9 KO Plasmid (m): sc-425749
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIMPL 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 SIMPL 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 | |
SIMPL CRISPR/Cas9 KO Plasmid (m) | sc-425749 | 20 µg | $397.00 |
Overview
Irak1bp1 encodes SIMPL (signaling molecule that interacts with Pelle-like kinase), a cytosolic adaptor implicated in Toll-like receptor and IL-1 receptor signaling downstream of IRAK1. SIMPL has been linked to modulation of NF-κB–dependent transcriptional programs that shape innate immune activation, inflammatory gene expression, and cellular stress responses. In mouse systems, perturbation of SIMPL-associated signaling can influence cytokine-driven pathways relevant to chronic inflammation and immune dysregulation phenotypes. These properties make Irak1bp1 a useful target for dissecting stimulus-dependent NF-κB signaling dynamics and cross-talk with other inflammatory pathways in myeloid and stromal cell models.
SIMPL CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Irak1bp1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Irak1bp1 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 Irak1bp1 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 SIMPL protein expression.
This CRISPR knockout system enables efficient generation of Irak1bp1-deficient cell models for investigation of SIMPL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Irak1bp1 exon(s) critical for SIMPL 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 Irak1bp1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SIMPL CRISPR/Cas9 KO Plasmid (m) and SIMPL CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Irak1bp1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SIMPL HDR Plasmid (m) and SIMPL HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Irak1bp1 homology arms to support homology-directed repair at defined Irak1bp1 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.