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.
DLK2 CRISPR/Cas9 KO Plasmid (h): sc-406327
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DLK2 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 DLK2 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: DLK2 Antibody (B-10): sc-376896
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DLK2 CRISPR/Cas9 KO Plasmid (h) | sc-406327 | 20 µg | $397.00 |
Overview
DLK2 (delta like non-canonical Notch ligand 2) encodes a transmembrane protein with EGF-like repeats that functions as an atypical ligand/modulator of Notch signaling. In human cells, DLK2 can influence cell–cell communication programs that govern lineage commitment, differentiation, and tissue patterning, intersecting with pathways that shape progenitor states and epithelial–mesenchymal dynamics. Altered expression of DLK2 has been reported in multiple tumor contexts and developmental biology models, supporting investigation of its contribution to proliferation control, stem-like phenotypes, and microenvironmental signaling. DLK2 is therefore useful for dissecting non-canonical Notch pathway regulation and downstream transcriptional responses.
DLK2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DLK2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DLK2 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 DLK2 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 DLK2 protein expression.
This CRISPR knockout system enables efficient generation of DLK2-deficient cell models for investigation of DLK2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting DLK2 exon(s) critical for DLK2 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 DLK2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by DLK2 CRISPR/Cas9 KO Plasmid (h) and DLK2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DLK2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by DLK2 HDR Plasmid (h) and DLK2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DLK2 homology arms to support homology-directed repair at defined DLK2 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.