Scleraxis CRISPR/Cas9 KO Plasmid (m): sc-422833
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Scleraxis 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 Scleraxis 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 | |
Scleraxis CRISPR/Cas9 KO Plasmid (m) | sc-422833 | 20 µg | $397.00 |
Overview
Scx encodes scleraxis, a basic helix–loop–helix transcription factor that functions as a lineage-determining regulator of tendon and ligament development. Scleraxis coordinates extracellular matrix gene programs and tenogenic differentiation, integrating cues from mechanotransduction and growth factor pathways such as TGF-β and related signaling networks that shape fibroblast identity and matrix remodeling. In mouse models, Scx activity is closely linked to connective tissue homeostasis, influencing collagen organization, cell migration, and tissue maturation during development and repair. Dysregulation of Scx-associated transcriptional programs is relevant to studies of tendinopathy, fibrosis-like matrix remodeling, and musculoskeletal injury responses.
Scleraxis CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Scx gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Scx 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 Scx 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 Scleraxis protein expression.
This CRISPR knockout system enables efficient generation of Scx-deficient cell models for investigation of Scleraxis signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Scx exon(s) critical for Scleraxis 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 Scx genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Scleraxis CRISPR/Cas9 KO Plasmid (m) and Scleraxis CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Scx locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Scleraxis HDR Plasmid (m) and Scleraxis HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Scx homology arms to support homology-directed repair at defined Scx 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.