Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
RGS7 CRISPR/Cas9 KO Plasmid (h): sc-406720
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RGS7 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 RGS7 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 | |
RGS7 CRISPR/Cas9 KO Plasmid (h) | sc-406720 | 20 µg | $397.00 |
Overview
RGS7 (Regulator of G protein signaling 7) is a GTPase-activating protein that accelerates termination of GPCR signaling by promoting Gα subunit GTP hydrolysis, particularly in Gi/o-coupled pathways. It functions prominently in neuronal signaling complexes, often in association with Gβ5 and membrane anchors such as R7BP, shaping synaptic transmission, cAMP dynamics, and ion channel modulation. Through its control of GPCR effector pathways, RGS7 influences neurotransmitter responses and activity-dependent signaling programs in the nervous system. Dysregulation of RGS7-linked signaling has been investigated in the context of neuropsychiatric and neurodegenerative disease mechanisms where altered GPCR tone and synaptic homeostasis are implicated.
RGS7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RGS7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RGS7 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 RGS7 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 RGS7 protein expression.
This CRISPR knockout system enables efficient generation of RGS7-deficient cell models for investigation of RGS7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RGS7 exon(s) critical for RGS7 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 RGS7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RGS7 CRISPR/Cas9 KO Plasmid (h) and RGS7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RGS7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RGS7 HDR Plasmid (h) and RGS7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RGS7 homology arms to support homology-directed repair at defined RGS7 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.