Ral B CRISPR/Cas9 KO Plasmid (m): sc-425679
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Ral B 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 Ral B 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: Ral B Antibody (C-8): sc-390108
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ral B CRISPR/Cas9 KO Plasmid (m) | sc-425679 | 20 µg | $397.00 |
Overview
Ralb encodes the small GTPase Ral B, a Ras-like molecular switch that cycles between GDP- and GTP-bound states to regulate membrane trafficking and cytoskeletal remodeling. Ral B signals through effectors such as the exocyst complex and RalBP1 to control vesicle docking, endocytosis, cell polarity, and cytokinesis, and it can interface with stress and innate immune signaling through pathways linked to TBK1 activation. Through these processes, Ral B influences cellular proliferation, migration, and survival programs that are frequently studied in the context of oncogenic Ras network output and tumor cell invasion. In mouse models, Ralb perturbation supports mechanistic investigation of small GTPase signaling nodes implicated in cancer biology and inflammation-associated phenotypes.
Ral B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ralb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ralb 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 Ralb 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 Ral B protein expression.
This CRISPR knockout system enables efficient generation of Ralb-deficient cell models for investigation of Ral B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ralb exon(s) critical for Ral B 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 Ralb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Ral B CRISPR/Cas9 KO Plasmid (m) and Ral B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ralb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Ral B HDR Plasmid (m) and Ral B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ralb homology arms to support homology-directed repair at defined Ralb 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.