GAP1m CRISPR/Cas9 KO Plasmid (m): sc-431130
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GAP1m 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 GAP1m 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GAP1m Antibody (15): sc-135916
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GAP1m CRISPR/Cas9 KO Plasmid (m) | sc-431130 | 20 µg | $397.00 |
Overview
Rasa2 encodes the Ras GTPase-activating protein GAP1m, a negative regulator of Ras signaling that accelerates GTP hydrolysis to constrain MAPK/ERK and PI3K/AKT pathway output. By tuning the amplitude and duration of Ras activity, GAP1m influences cell-cycle progression, differentiation cues, and cytoskeletal dynamics that shape migration and adhesion. In mouse models, altered Rasa2 function has been associated with dysregulated growth-factor signaling and aberrant immune and developmental phenotypes, making it relevant for studying Ras-driven network rewiring in disease-relevant contexts. Its position as a signaling brake supports mechanistic investigations of pathway feedback, signal integration, and context-dependent Ras effector engagement.
GAP1m CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rasa2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rasa2 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 Rasa2 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 GAP1m protein expression.
This CRISPR knockout system enables efficient generation of Rasa2-deficient cell models for investigation of GAP1m signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rasa2 exon(s) critical for GAP1m 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 Rasa2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GAP1m CRISPR/Cas9 KO Plasmid (m) and GAP1m CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rasa2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GAP1m HDR Plasmid (m) and GAP1m HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rasa2 homology arms to support homology-directed repair at defined Rasa2 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.