RGS17 CRISPR/Cas9 KO Plasmid (m): sc-425225
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RGS17 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 RGS17 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 | |
RGS17 CRISPR/Cas9 KO Plasmid (m) | sc-425225 | 20 µg | $397.00 |
Overview
Rgs17 encodes regulator of G protein signaling 17 (RGS17), a member of the RGS family that accelerates GTP hydrolysis on Gα subunits to terminate GPCR-driven signaling. By dampening heterotrimeric G protein activity, RGS17 influences cAMP/PKA signaling, downstream kinase cascades, and transcriptional programs linked to neuronal communication and secretory cell responses. In mouse systems, altered Rgs17 expression has been associated with changes in neurobehavioral phenotypes and with dysregulated signaling networks that are commonly interrogated in models of tumor biology and metastasis. These properties make RGS17 a useful node for studying GPCR signal amplitude, pathway cross-talk, and context-dependent transcriptional outputs.
RGS17 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rgs17 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rgs17 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 Rgs17 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 RGS17 protein expression.
This CRISPR knockout system enables efficient generation of Rgs17-deficient cell models for investigation of RGS17 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rgs17 exon(s) critical for RGS17 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 Rgs17 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RGS17 CRISPR/Cas9 KO Plasmid (m) and RGS17 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rgs17 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RGS17 HDR Plasmid (m) and RGS17 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rgs17 homology arms to support homology-directed repair at defined Rgs17 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.