GRP CRISPR/Cas9 KO Plasmid (h): sc-402811
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GRP 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 GRP 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: GRP Antibody (E-11): sc-271045
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GRP CRISPR/Cas9 KO Plasmid (h) | sc-402811 | 20 µg | $397.00 |
Overview
Gastrin-releasing peptide (GRP) is a neuropeptide that signals through the bombesin receptor family, primarily GRPR, to regulate intracellular calcium flux, phospholipase C activity, and downstream MAPK/ERK and PI3K-AKT signaling. In human tissues, GRP contributes to neuroendocrine communication, epithelial homeostasis, and modulation of secretory and contractile responses. Dysregulated GRP–GRPR signaling has been associated with altered proliferation, migration, and neuroinflammatory responses, making GRP a relevant node in studies of oncogenic signaling and tumor–microenvironment crosstalk. GRP expression and processing also intersect with peptide hormone maturation and regulated secretion pathways, supporting its use as a marker for neuroendocrine states and signaling plasticity.
GRP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GRP gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GRP 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 GRP 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 GRP protein expression.
This CRISPR knockout system enables efficient generation of GRP-deficient cell models for investigation of GRP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GRP exon(s) critical for GRP 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 GRP genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GRP CRISPR/Cas9 KO Plasmid (h) and GRP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GRP locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GRP HDR Plasmid (h) and GRP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GRP homology arms to support homology-directed repair at defined GRP 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.