PTPβ CRISPR/Cas9 KO Plasmid (h): sc-402100
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PTPβ 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 PTPβ 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 | |
PTPβ CRISPR/Cas9 KO Plasmid (h) | sc-402100 | 20 µg | $397.00 |
Overview
PTPRB encodes the receptor-type protein tyrosine phosphatase beta (PTPβ), an endothelial-enriched phosphatase that counterbalances receptor tyrosine kinase signaling to modulate vascular development, barrier function, and angiogenic responses. By dephosphorylating signaling nodes linked to VEGF/FGF pathways and junctional remodeling, PTPβ helps tune endothelial cell migration, permeability, and vessel stabilization. Altered PTPRB activity or expression has been associated with dysregulated angiogenesis and vascular homeostasis, making it relevant to studies of inflammation-associated vascular leakage and tumor-associated neovascularization. Its regulatory role in phosphorylation-dependent signaling also supports mechanistic investigations of endothelial differentiation and microvascular network formation.
PTPβ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PTPRB gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PTPRB 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 PTPRB 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 PTPβ protein expression.
This CRISPR knockout system enables efficient generation of PTPRB-deficient cell models for investigation of PTPβ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PTPRB exon(s) critical for PTPβ 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 PTPRB genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PTPβ CRISPR/Cas9 KO Plasmid (h) and PTPβ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PTPRB locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PTPβ HDR Plasmid (h) and PTPβ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PTPRB homology arms to support homology-directed repair at defined PTPRB 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.