SIRT2 CRISPR/Cas9 KO Plasmid (m): sc-425703
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SIRT2 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 SIRT2 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: SIRT2 Antibody (A-5): sc-28298
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SIRT2 CRISPR/Cas9 KO Plasmid (m) | sc-425703 | 20 µg | $397.00 |
Overview
Sirt2 encodes the NAD⁺-dependent deacetylase SIRT2, a primarily cytosolic sirtuin that regulates acetylation of proteins involved in microtubule dynamics, cell-cycle progression, and metabolic homeostasis. SIRT2 modulates key processes including mitotic checkpoint control, autophagy, and oxidative stress responses, linking nutrient sensing to mitochondrial and cytoskeletal function. In mouse systems, SIRT2 activity has been associated with pathways relevant to neurodegeneration, inflammation, and metabolic dysregulation, making it a useful node for interrogating tissue-specific stress resilience. Altered SIRT2-dependent deacetylation can influence transcriptional programs and proteostasis networks that shape susceptibility to age-related phenotypes in vivo and in primary cell models.
SIRT2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sirt2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sirt2 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 Sirt2 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 SIRT2 protein expression.
This CRISPR knockout system enables efficient generation of Sirt2-deficient cell models for investigation of SIRT2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sirt2 exon(s) critical for SIRT2 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 Sirt2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SIRT2 CRISPR/Cas9 KO Plasmid (m) and SIRT2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sirt2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SIRT2 HDR Plasmid (m) and SIRT2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sirt2 homology arms to support homology-directed repair at defined Sirt2 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.