SARM CRISPR/Cas9 KO Plasmid (h): sc-403427
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SARM 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 SARM 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 | |
SARM CRISPR/Cas9 KO Plasmid (h) | sc-403427 | 20 µg | $397.00 |
Overview
Sterile alpha and TIR motif–containing 1 (SARM1; SARM) is an axon-enriched innate immune adaptor and NADase that functions as a central executioner of programmed axon degeneration. Upon neuronal injury or metabolic stress, SARM1 activation promotes rapid NAD+ depletion, energetic failure, and cytoskeletal breakdown, integrating with pathways that regulate NMN/NAD homeostasis, mitochondrial dysfunction, calcium influx, and MAPK signaling. Dysregulated SARM1 activity has been implicated in neurodegenerative and neuroinflammatory contexts, including peripheral neuropathies and axonopathy-linked disorders, where axonal maintenance and stress responses are compromised. As a signaling node connecting TIR-domain biology with metabolic collapse, SARM1 is widely studied for its roles in axon integrity, neuronal survival, and innate immune-associated signaling.
SARM CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SARM1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SARM1 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 SARM1 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 SARM protein expression.
This CRISPR knockout system enables efficient generation of SARM1-deficient cell models for investigation of SARM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SARM1 exon(s) critical for SARM 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 SARM1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SARM CRISPR/Cas9 KO Plasmid (h) and SARM CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SARM1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SARM HDR Plasmid (h) and SARM HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SARM1 homology arms to support homology-directed repair at defined SARM1 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.