SENP2 CRISPR/Cas9 KO Plasmid (m): sc-429217
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SENP2 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 SENP2 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 | |
SENP2 CRISPR/Cas9 KO Plasmid (m) | sc-429217 | 20 µg | $397.00 |
Overview
Senp2 encodes sentrin/SUMO-specific protease 2 (SENP2), a deSUMOylating enzyme that reverses SUMO conjugation to regulate protein stability, subcellular localization, and transcriptional programs. SENP2 activity shapes SUMO-dependent control of cell-cycle progression, DNA damage responses, and nuclear transport, influencing signaling nodes such as NF-κB and p53-associated stress pathways. In mouse systems, Senp2 has been linked to developmental and cardiovascular phenotypes and is frequently studied for its impact on inflammation, metabolic regulation, and cellular homeostasis. Dysregulated SUMO protease function can perturb proteostasis and chromatin-associated processes that are relevant to disease modeling and pathway interrogation.
SENP2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Senp2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Senp2 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 Senp2 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 SENP2 protein expression.
This CRISPR knockout system enables efficient generation of Senp2-deficient cell models for investigation of SENP2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Senp2 exon(s) critical for SENP2 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 Senp2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SENP2 CRISPR/Cas9 KO Plasmid (m) and SENP2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Senp2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SENP2 HDR Plasmid (m) and SENP2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Senp2 homology arms to support homology-directed repair at defined Senp2 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.