TREM-1 CRISPR/Cas9 KO Plasmid (m): sc-425490
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TREM-1 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 TREM-1 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 | |
TREM-1 CRISPR/Cas9 KO Plasmid (m) | sc-425490 | 20 µg | $397.00 |
Overview
Triggering receptor expressed on myeloid cells 1 (TREM-1) is an immunoreceptor predominantly found on neutrophils and monocytes/macrophages that amplifies inflammatory responses initiated by pattern-recognition receptors. In mouse, TREM-1 signaling integrates with adaptor-mediated pathways to potentiate NF-κB and MAPK activation, increasing production of proinflammatory cytokines and chemokines and reinforcing innate immune effector functions. Trem1 activity is closely linked to myeloid cell recruitment, activation, and crosstalk with endothelial and stromal compartments during acute and chronic inflammation. Dysregulated TREM-1 signaling has been associated with inflammatory and infectious disease models, as well as tumor-associated myeloid phenotypes and tissue damage pathways driven by excessive cytokine responses.
TREM-1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trem1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trem1 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 Trem1 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 TREM-1 protein expression.
This CRISPR knockout system enables efficient generation of Trem1-deficient cell models for investigation of TREM-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trem1 exon(s) critical for TREM-1 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 Trem1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TREM-1 CRISPR/Cas9 KO Plasmid (m) and TREM-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trem1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TREM-1 HDR Plasmid (m) and TREM-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trem1 homology arms to support homology-directed repair at defined Trem1 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.