VEGF-B CRISPR/Cas9 KO Plasmid (m): sc-423666
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VEGF-B 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 VEGF-B 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-B Antibody (RM0008-6E72): sc-101582
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VEGF-B CRISPR/Cas9 KO Plasmid (m) | sc-423666 | 20 µg | $397.00 |
Overview
Vegfb encodes vascular endothelial growth factor B (VEGF-B), a secreted VEGF family ligand that primarily signals through VEGFR1 (FLT1) and neuropilins to modulate endothelial cell behavior and vascular homeostasis. In contrast to strongly angiogenic VEGF-A, VEGF-B is frequently linked to endothelial survival, vessel stabilization, and regulation of lipid uptake and metabolism in tissues with high oxidative demand. VEGF-B–dependent signaling intersects with PI3K–AKT and MAPK pathways and can influence mitochondrial function and fatty acid transport programs. Altered VEGF-B activity has been studied in contexts of metabolic stress and cardiovascular biology, including vascular dysfunction and tissue susceptibility to ischemic injury.
VEGF-B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Vegfb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Vegfb 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 Vegfb 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-B protein expression.
This CRISPR knockout system enables efficient generation of Vegfb-deficient cell models for investigation of VEGF-B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Vegfb exon(s) critical for VEGF-B 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 Vegfb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VEGF-B CRISPR/Cas9 KO Plasmid (m) and VEGF-B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Vegfb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VEGF-B HDR Plasmid (m) and VEGF-B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Vegfb homology arms to support homology-directed repair at defined Vegfb 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.