Dexras1 CRISPR/Cas9 KO Plasmid (m): sc-422604
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Dexras1 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 Dexras1 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 | |
Dexras1 CRISPR/Cas9 KO Plasmid (m) | sc-422604 | 20 µg | $397.00 |
Overview
Rasd1 encodes Dexras1, a small Ras-related GTPase that functions as a signaling switch linking extracellular cues to intracellular second-messenger pathways in mouse cells. Dexras1 has been implicated in modulation of heterotrimeric G-protein signaling and cAMP-dependent responses, and it participates in neuronal activity–associated programs influenced by glucocorticoids and nitric oxide–related signaling. Through these roles, Rasd1 can shape transcriptional outputs and cellular adaptation to stress and hormonal inputs. Dysregulated Rasd1/Dexras1 signaling has been studied in the context of neuroendocrine regulation and nervous system phenotypes, making it relevant for mechanistic investigations of signaling-dependent gene regulation.
Dexras1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rasd1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rasd1 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 Rasd1 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 Dexras1 protein expression.
This CRISPR knockout system enables efficient generation of Rasd1-deficient cell models for investigation of Dexras1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rasd1 exon(s) critical for Dexras1 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 Rasd1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Dexras1 CRISPR/Cas9 KO Plasmid (m) and Dexras1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rasd1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Dexras1 HDR Plasmid (m) and Dexras1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rasd1 homology arms to support homology-directed repair at defined Rasd1 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.