TARC CRISPR/Cas9 KO Plasmid (m): sc-422837
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TARC 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 TARC 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 | |
TARC CRISPR/Cas9 KO Plasmid (m) | sc-422837 | 20 µg | $397.00 |
Overview
Ccl17 encodes thymus and activation-regulated chemokine (TARC/CCL17), a secreted CC chemokine that binds CCR4 to direct chemotaxis of CCR4-positive T cell subsets, including Th2 cells and regulatory T cells. In mouse immune tissues, TARC contributes to leukocyte trafficking, shaping the composition and polarization of inflammatory infiltrates and coordinating antigen-driven responses. Ccl17 expression is commonly induced downstream of cytokine signaling and pattern-recognition receptor activation in myeloid and stromal compartments, linking innate cues to adaptive cell recruitment. Dysregulated Ccl17/TARC signaling is associated with allergic-type inflammation and immune-mediated pathology, making it a useful node for studying chemokine gradients, barrier inflammation, and T cell–myeloid crosstalk.
TARC CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccl17 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccl17 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 Ccl17 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 TARC protein expression.
This CRISPR knockout system enables efficient generation of Ccl17-deficient cell models for investigation of TARC signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccl17 exon(s) critical for TARC 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 Ccl17 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TARC CRISPR/Cas9 KO Plasmid (m) and TARC CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccl17 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TARC HDR Plasmid (m) and TARC HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccl17 homology arms to support homology-directed repair at defined Ccl17 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.