ACMSD CRISPR/Cas9 KO Plasmid (m): sc-435223
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACMSD 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 ACMSD 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 | |
ACMSD CRISPR/Cas9 KO Plasmid (m) | sc-435223 | 20 µg | $397.00 |
Overview
Acmsd encodes aminocarboxymuconate semialdehyde decarboxylase (ACMSD), a key enzyme in the kynurenine pathway of tryptophan catabolism that diverts intermediates away from quinolinate formation and influences de novo NAD⁺ biosynthesis. By regulating the balance between picolinic acid and quinolinic acid production, ACMSD can impact cellular redox metabolism, mitochondrial function, and inflammatory signaling linked to amino acid sensing. Altered kynurenine pathway flux has been associated with neuroinflammation, excitotoxic stress, and metabolic dysregulation, making Acmsd a useful target for mechanistic studies in CNS and peripheral tissues. In mouse models, perturbing Acmsd supports investigation of how tryptophan-derived metabolites shape immune–metabolic crosstalk and tissue homeostasis.
ACMSD CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Acmsd gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Acmsd 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 Acmsd 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 ACMSD protein expression.
This CRISPR knockout system enables efficient generation of Acmsd-deficient cell models for investigation of ACMSD signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Acmsd exon(s) critical for ACMSD 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 Acmsd genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACMSD CRISPR/Cas9 KO Plasmid (m) and ACMSD CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Acmsd locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACMSD HDR Plasmid (m) and ACMSD HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Acmsd homology arms to support homology-directed repair at defined Acmsd 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.