ALX3 CRISPR/Cas9 KO Plasmid (m): sc-419094
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ALX3 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 ALX3 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 | |
ALX3 CRISPR/Cas9 KO Plasmid (m) | sc-419094 | 20 µg | $397.00 |
Overview
Alx3 encodes the ALX3 homeobox transcription factor, a nuclear regulator required for craniofacial and anterior head patterning during embryogenesis. ALX3 influences gene expression programs controlling neural crest cell specification, mesenchymal differentiation, and morphogenetic processes that shape craniofacial structures. Through its DNA-binding homeodomain, ALX3 integrates developmental signaling inputs to coordinate lineage-restricted transcriptional networks. Dysregulated ALX family activity has been linked to congenital craniofacial abnormalities, making Alx3 a relevant target for mechanistic studies of developmental gene regulation.
ALX3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Alx3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Alx3 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 Alx3 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 ALX3 protein expression.
This CRISPR knockout system enables efficient generation of Alx3-deficient cell models for investigation of ALX3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Alx3 exon(s) critical for ALX3 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 Alx3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ALX3 CRISPR/Cas9 KO Plasmid (m) and ALX3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Alx3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ALX3 HDR Plasmid (m) and ALX3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Alx3 homology arms to support homology-directed repair at defined Alx3 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.