PTPε CRISPR/Cas9 KO Plasmid (h): sc-405606
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PTPε 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 PTPε 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: PTPε Antibody (G-2): sc-515692
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PTPε CRISPR/Cas9 KO Plasmid (h) | sc-405606 | 20 µg | $397.00 |
Overview
PTPRE encodes protein tyrosine phosphatase epsilon (PTPε), a receptor-type and cytosolic phosphatase that modulates signaling by dephosphorylating phosphotyrosine residues on key kinase substrates. PTPε participates in control of MAPK and JAK/STAT pathway output and can tune receptor tyrosine kinase and Src-family kinase signaling, influencing cell proliferation, adhesion, migration, and immune-cell activation thresholds. By shaping phosphorylation-dependent signaling networks, PTPε is studied in contexts of dysregulated growth factor signaling, inflammatory signaling, and oncogenic pathway rewiring. Its isoform-specific localization and activity make PTPRE a useful node for dissecting compartmentalized phosphatase control of cellular signaling.
PTPε CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PTPRE gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PTPRE 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 PTPRE 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 PTPε protein expression.
This CRISPR knockout system enables efficient generation of PTPRE-deficient cell models for investigation of PTPε signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PTPRE exon(s) critical for PTPε 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 PTPRE genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PTPε CRISPR/Cas9 KO Plasmid (h) and PTPε CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PTPRE locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PTPε HDR Plasmid (h) and PTPε HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PTPRE homology arms to support homology-directed repair at defined PTPRE 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.