CCL27 CRISPR/Cas9 KO Plasmid (m): sc-422842
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CCL27 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 CCL27 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: CCL27 Antibody (G-6): sc-390112
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CCL27 CRISPR/Cas9 KO Plasmid (m) | sc-422842 | 20 µg | $397.00 |
Overview
Ccl27a encodes the chemokine CCL27 (also known as CTACK), a skin-associated CC chemokine that helps coordinate leukocyte trafficking by forming gradients that guide CCR10-expressing T cells toward epithelial sites. CCL27 contributes to chemokine-driven cell migration, immune surveillance, and inflammatory signaling within the skin microenvironment, influencing interactions between keratinocytes and infiltrating lymphocytes. Dysregulated CCL27–CCR10 axis activity has been linked to cutaneous inflammation and altered immune cell recruitment in models of dermatitis-like disease processes. In mouse systems, Ccl27a is therefore widely studied to dissect mechanisms of tissue-selective chemotaxis and epithelial immune regulation.
CCL27 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccl27a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccl27a 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 Ccl27a 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 CCL27 protein expression.
This CRISPR knockout system enables efficient generation of Ccl27a-deficient cell models for investigation of CCL27 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccl27a exon(s) critical for CCL27 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 Ccl27a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CCL27 CRISPR/Cas9 KO Plasmid (m) and CCL27 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccl27a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CCL27 HDR Plasmid (m) and CCL27 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccl27a homology arms to support homology-directed repair at defined Ccl27a 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.