Rab 25 CRISPR/Cas9 KO Plasmid (m): sc-424753
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rab 25 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 Rab 25 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: Rab 25 Antibody (3F12F3): sc-65978
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rab 25 CRISPR/Cas9 KO Plasmid (m) | sc-424753 | 20 µg | $397.00 |
Overview
Rab25 encodes the small GTPase Rab 25, a Rab11 subfamily member that regulates membrane trafficking, including endocytic recycling and polarized transport of receptors and integrins in epithelial cells. Through control of vesicle budding, tethering, and fusion, Rab 25 influences cell polarity, migration, and signaling output from surface receptors that couple to pathways such as PI3K–AKT and growth factor receptor recycling. Dysregulated RAB25 activity has been linked to altered epithelial homeostasis and tumor-associated phenotypes in multiple tissues, making it relevant for studying invasion, metastasis-associated trafficking programs, and context-dependent oncogenic or tumor-suppressive functions. In mouse models, Rab25 perturbation supports mechanistic investigation of vesicular transport networks in development and disease-relevant cellular behaviors.
Rab 25 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rab25 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rab25 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 Rab25 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 Rab 25 protein expression.
This CRISPR knockout system enables efficient generation of Rab25-deficient cell models for investigation of Rab 25 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Rab25 exon(s) critical for Rab 25 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 Rab25 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Rab 25 CRISPR/Cas9 KO Plasmid (m) and Rab 25 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rab25 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Rab 25 HDR Plasmid (m) and Rab 25 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rab25 homology arms to support homology-directed repair at defined Rab25 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.