
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
N-Ras CRISPR/Cas9 KO Plasmid (m) | sc-421960 | 20 µg | $397.00 |
Mouse Nras encodes N-Ras, a membrane-associated small GTPase that cycles between GDP- and GTP-bound states to transduce signals from receptor tyrosine kinases and other upstream cues. Activated N-Ras engages core Ras effector pathways including RAF–MEK–ERK (MAPK) and PI3K–AKT, coordinating proliferation, differentiation, cytoskeletal dynamics, and survival. Tight control of N-Ras activity is essential for normal hematopoietic and developmental signaling, and perturbation of Ras pathway flux is broadly relevant to oncogenic transformation and inflammatory microenvironment responses. Nras therefore serves as a key node for dissecting Ras-driven network rewiring and pathway crosstalk in mouse cellular and disease models.
N-Ras CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Nras gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Nras 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 Nras 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 N-Ras protein expression.
This CRISPR knockout system enables efficient generation of Nras-deficient cell models for investigation of N-Ras signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.