RPTPα CRISPR/Cas9 KO Plasmid (m): sc-422515
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RPTPα 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 RPTPα 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: RPTPα Antibody (H-4): sc-398203
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RPTPα CRISPR/Cas9 KO Plasmid (m) | sc-422515 | 20 µg | $397.00 |
Overview
Mouse Ptpra encodes receptor-type protein tyrosine phosphatase alpha (RPTPα), a transmembrane phosphatase that modulates signaling by dephosphorylating inhibitory tyrosine residues on Src family kinases and related substrates. Through this activity it influences integrin-mediated adhesion, focal adhesion dynamics, cytoskeletal remodeling, and downstream MAPK/ERK signaling that collectively shape proliferation, migration, and differentiation programs. RPTPα also interfaces with receptor tyrosine kinase crosstalk and can tune signaling thresholds in neuronal and immune-related contexts. Dysregulated Ptpra signaling has been linked to processes relevant to oncogenic transformation and invasive behavior, making it a useful node for mechanistic studies of kinase/phosphatase balance in disease-associated pathways.
RPTPα CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ptpra gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ptpra 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 Ptpra 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 RPTPα protein expression.
This CRISPR knockout system enables efficient generation of Ptpra-deficient cell models for investigation of RPTPα signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ptpra exon(s) critical for RPTPα 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 Ptpra genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RPTPα CRISPR/Cas9 KO Plasmid (m) and RPTPα CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ptpra locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RPTPα HDR Plasmid (m) and RPTPα HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ptpra homology arms to support homology-directed repair at defined Ptpra 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.