VEGF CRISPR/Cas9 KO Plasmid (r): sc-437276
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VEGF CRISPR/Cas9 Knockout (KO) Plasmid (r) 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 VEGF 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: VEGF Antibody (C-1): sc-7269
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VEGF CRISPR/Cas9 KO Plasmid (r) | sc-437276 | 20 µg | $397.00 |
Overview
Vascular endothelial growth factor (VEGF) is a secreted, heparin-binding signaling protein that drives angiogenesis and vascular permeability by activating receptor tyrosine kinases such as VEGFR2 on endothelial cells. VEGF signaling propagates through PI3K–AKT, MAPK/ERK, and PLCγ–PKC pathways to regulate endothelial proliferation, migration, survival, and nitric oxide–linked permeability responses. It also interfaces with hypoxia-inducible factor (HIF) programs and extracellular matrix remodeling to coordinate tissue vascularization during development and stress. Dysregulated VEGF activity is widely used as a mechanistic readout in models of pathological neovascularization, inflammation-associated edema, ischemia-related remodeling, and tumor-associated angiogenesis.
VEGF CRISPR/Cas9 KO Plasmid (r) is a pool of plasmids designed for targeted disruption of the gene in rat cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the 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 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 VEGF protein expression.
This CRISPR knockout system enables efficient generation of -deficient cell models for investigation of VEGF signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting exon(s) critical for VEGF 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 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VEGF CRISPR/Cas9 KO Plasmid (r) and VEGF CRISPR/Cas9 KO Plasmid (r2) target distinct sites within the locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VEGF HDR Plasmid (r) and VEGF HDR Plasmid (r2) contain a puromycin resistance cassette and an RFP reporter flanked by homology arms to support homology-directed repair at defined 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.