VPAC1 CRISPR/Cas9 KO Plasmid (m): sc-423678
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VPAC1 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 VPAC1 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 | |
VPAC1 CRISPR/Cas9 KO Plasmid (m) | sc-423678 | 20 µg | $397.00 |
Overview
Vipr1 encodes VPAC1, a class B G protein–coupled receptor that binds vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase–activating polypeptide to couple predominantly to Gs and elevate intracellular cAMP. VPAC1 signaling engages PKA/CREB-dependent transcriptional programs and can intersect with MAPK and PI3K pathways to regulate cellular proliferation, differentiation, epithelial barrier function, and cytokine responses. In mouse tissues, VPAC1 contributes to neuroendocrine and immunoregulatory circuits, including modulation of inflammatory signaling and smooth muscle/secretory activity. Dysregulated VIP–VPAC1 axis has been implicated in models of inflammatory bowel disease, asthma-like airway inflammation, and tumor-associated microenvironment signaling, supporting mechanistic studies of GPCR-driven immune and epithelial processes.
VPAC1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Vipr1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Vipr1 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 Vipr1 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 VPAC1 protein expression.
This CRISPR knockout system enables efficient generation of Vipr1-deficient cell models for investigation of VPAC1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Vipr1 exon(s) critical for VPAC1 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 Vipr1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VPAC1 CRISPR/Cas9 KO Plasmid (m) and VPAC1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Vipr1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VPAC1 HDR Plasmid (m) and VPAC1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Vipr1 homology arms to support homology-directed repair at defined Vipr1 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.