VIP CRISPR/Cas9 KO Plasmid (m): sc-423677
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VIP 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 VIP 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 | |
VIP CRISPR/Cas9 KO Plasmid (m) | sc-423677 | 20 µg | $397.00 |
Overview
Vip encodes vasoactive intestinal peptide (VIP), a neuropeptide that signals primarily through the GPCRs VIPR1 and VIPR2 to stimulate adenylate cyclase, elevate cAMP, and activate PKA/CREB-dependent transcriptional programs. In mouse, VIP contributes to neuroendocrine communication, circadian rhythm coordination within the suprachiasmatic nucleus, and regulation of smooth muscle tone, vasodilation, and secretory activity across peripheral tissues. VIP-mediated signaling modulates immune cell polarization and cytokine production, linking this pathway to inflammatory homeostasis and mucosal barrier function. Dysregulated VIP/VIPR signaling has been associated with altered neuroinflammatory responses, gastrointestinal motility and secretion phenotypes, and context-dependent effects on tumor-associated immunity and neuroendocrine traits in disease models.
VIP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Vip gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Vip 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 Vip 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 VIP protein expression.
This CRISPR knockout system enables efficient generation of Vip-deficient cell models for investigation of VIP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Vip exon(s) critical for VIP 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 Vip genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by VIP CRISPR/Cas9 KO Plasmid (m) and VIP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Vip locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by VIP HDR Plasmid (m) and VIP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Vip homology arms to support homology-directed repair at defined Vip 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.