Ras-GRF2 CRISPR/Cas9 KO Plasmid (h): sc-404141
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ras-GRF2 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 Ras-GRF2 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 | |
Ras-GRF2 CRISPR/Cas9 KO Plasmid (h) | sc-404141 | 20 µg | $397.00 |
Overview
RASGRF2 encodes Ras-GRF2, a calcium- and phospholipid-regulated guanine nucleotide exchange factor that activates Ras and related small GTPases to control MAPK/ERK signaling dynamics. Ras-GRF2 integrates inputs from neuronal activity and receptor-mediated signaling to influence synaptic plasticity, neurite outgrowth, and cytoskeletal remodeling through downstream kinases and Rho family pathways. By modulating Ras-dependent transcriptional programs, RASGRF2 impacts cellular proliferation and differentiation states in a context-dependent manner. Dysregulated Ras pathway coupling involving Ras-GRF2 has been investigated in neurobiology and cancer-related signaling models where altered GTPase activation can reshape growth and survival responses.
Ras-GRF2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RASGRF2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RASGRF2 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 RASGRF2 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 Ras-GRF2 protein expression.
This CRISPR knockout system enables efficient generation of RASGRF2-deficient cell models for investigation of Ras-GRF2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RASGRF2 exon(s) critical for Ras-GRF2 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 RASGRF2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Ras-GRF2 CRISPR/Cas9 KO Plasmid (h) and Ras-GRF2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RASGRF2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Ras-GRF2 HDR Plasmid (h) and Ras-GRF2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RASGRF2 homology arms to support homology-directed repair at defined RASGRF2 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.