SSTR5 CRISPR/Cas9 KO Plasmid (h): sc-404199
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SSTR5 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 SSTR5 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 | |
SSTR5 CRISPR/Cas9 KO Plasmid (h) | sc-404199 | 20 µg | $397.00 |
Overview
Somatostatin receptor 5 (SSTR5) is a G protein–coupled receptor for somatostatin that predominantly couples to Gi/o proteins to suppress adenylyl cyclase activity, reduce intracellular cAMP, and modulate ion channel signaling. Through downstream effects on MAPK/ERK and other GPCR-regulated pathways, SSTR5 influences hormone secretion, neurotransmission, and proliferation programs in a cell type–dependent manner. In human tissues, SSTR5 contributes to endocrine and metabolic regulation, including modulation of insulin and growth hormone axis signaling. Dysregulated somatostatin receptor signaling has been associated with altered secretory phenotypes and proliferative behavior in multiple disease-relevant contexts, making SSTR5 a useful node for pathway interrogation.
SSTR5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SSTR5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SSTR5 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 SSTR5 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 SSTR5 protein expression.
This CRISPR knockout system enables efficient generation of SSTR5-deficient cell models for investigation of SSTR5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SSTR5 exon(s) critical for SSTR5 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 SSTR5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SSTR5 CRISPR/Cas9 KO Plasmid (h) and SSTR5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SSTR5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SSTR5 HDR Plasmid (h) and SSTR5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SSTR5 homology arms to support homology-directed repair at defined SSTR5 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.