SULT1A1 CRISPR/Cas9 KO Plasmid (m): sc-423199
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SULT1A1 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 SULT1A1 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: SULT1A1 Antibody (214E2Z): sc-517645
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SULT1A1 CRISPR/Cas9 KO Plasmid (m) | sc-423199 | 20 µg | $397.00 |
Overview
Mouse Sult1a1 encodes the cytosolic sulfotransferase SULT1A1, a phase II xenobiotic-metabolizing enzyme that catalyzes the sulfonation of phenolic compounds using 3′-phosphoadenosine-5′-phosphosulfate (PAPS) as the sulfate donor. This reaction increases substrate polarity to influence cellular clearance, bioavailability, and chemical reactivity, integrating with broader detoxification networks that include cytochrome P450 oxidation and conjugation pathways. SULT1A1 activity shapes hepatic and extrahepatic handling of dietary constituents, environmental chemicals, and select signaling molecules, thereby affecting oxidative stress responses and metabolite-driven signaling. Altered sulfation capacity has been linked to variability in toxicant sensitivity and inflammation-associated tissue injury in disease-relevant models of liver and gastrointestinal physiology.
SULT1A1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sult1a1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sult1a1 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 Sult1a1 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 SULT1A1 protein expression.
This CRISPR knockout system enables efficient generation of Sult1a1-deficient cell models for investigation of SULT1A1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sult1a1 exon(s) critical for SULT1A1 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 Sult1a1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SULT1A1 CRISPR/Cas9 KO Plasmid (m) and SULT1A1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sult1a1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SULT1A1 HDR Plasmid (m) and SULT1A1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sult1a1 homology arms to support homology-directed repair at defined Sult1a1 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.