Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TECK CRISPR/Cas9 KO Plasmid (m): sc-422841
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TECK 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 TECK 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: TECK Antibody (YY05): sc-80344
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TECK CRISPR/Cas9 KO Plasmid (m) | sc-422841 | 20 µg | $397.00 |
Overview
Ccl25 encodes thymus-expressed chemokine (TECK), a CC chemokine that signals primarily through CCR9 to direct chemotactic migration and positioning of CCR9+ leukocytes. In mouse, TECK contributes to immune cell trafficking within thymic microenvironments and mucosal tissues, shaping lymphocyte homing, tissue surveillance, and regional immune organization. Downstream signaling engages GPCR-dependent pathways including PI3K/AKT and MAPK cascades that regulate motility, adhesion, and cytoskeletal remodeling. Dysregulated Ccl25–CCR9 axis activity has been implicated in inflammatory immune infiltration and altered lymphocyte localization relevant to mucosal inflammation and tumor-associated immune cell distribution models.
TECK CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccl25 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccl25 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 Ccl25 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 TECK protein expression.
This CRISPR knockout system enables efficient generation of Ccl25-deficient cell models for investigation of TECK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccl25 exon(s) critical for TECK 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 Ccl25 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TECK CRISPR/Cas9 KO Plasmid (m) and TECK CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccl25 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TECK HDR Plasmid (m) and TECK HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccl25 homology arms to support homology-directed repair at defined Ccl25 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.