Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
SENP3 CRISPR/Cas9 KO Plasmid (h): sc-403747
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SENP3 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 SENP3 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: SENP3 Antibody (E-7): sc-137219
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SENP3 CRISPR/Cas9 KO Plasmid (h) | sc-403747 | 20 µg | $397.00 |
Overview
SENP3 encodes a SUMO-specific protease that preferentially deconjugates SUMO2/3 from target proteins, shaping the dynamics of reversible SUMOylation. SENP3 localizes predominantly to the nucleolus and participates in ribosome biogenesis, nucleolar homeostasis, and regulation of transcriptional programs linked to cellular stress responses. Through modulation of SUMO-dependent protein interactions, SENP3 influences processes such as DNA damage signaling, cell-cycle control, and chromatin-associated regulation. Dysregulated SENP3 activity and SUMO pathway imbalance have been associated with altered proliferative signaling and genome maintenance defects relevant to cancer biology and other stress-linked pathologies.
SENP3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SENP3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SENP3 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 SENP3 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 SENP3 protein expression.
This CRISPR knockout system enables efficient generation of SENP3-deficient cell models for investigation of SENP3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SENP3 exon(s) critical for SENP3 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 SENP3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SENP3 CRISPR/Cas9 KO Plasmid (h) and SENP3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SENP3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SENP3 HDR Plasmid (h) and SENP3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SENP3 homology arms to support homology-directed repair at defined SENP3 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.