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.
SULT2A1 CRISPR/Cas9 KO Plasmid (m): sc-423184
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SULT2A1 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 SULT2A1 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 | |
SULT2A1 CRISPR/Cas9 KO Plasmid (m) | sc-423184 | 20 µg | $397.00 |
Overview
Mouse Sult2a1 encodes the cytosolic sulfotransferase SULT2A1, an enzyme that catalyzes 3′-phosphoadenosine-5′-phosphosulfate (PAPS)-dependent sulfonation of hydroxysteroids and bile acid intermediates. This phase II conjugation reaction modulates steroid and oxysterol bioavailability, facilitates detoxification, and supports hepatic and intestinal metabolic homeostasis. SULT2A1 activity intersects with bile acid and steroid hormone handling pathways and can influence xenobiotic metabolism through coordinated regulation with nuclear receptor programs such as FXR and PXR. Altered sulfation capacity is relevant to studies of cholestatic stress, liver inflammation, and endocrine/metabolic phenotypes in mouse models.
SULT2A1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sult2a1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sult2a1 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 Sult2a1 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 SULT2A1 protein expression.
This CRISPR knockout system enables efficient generation of Sult2a1-deficient cell models for investigation of SULT2A1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sult2a1 exon(s) critical for SULT2A1 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 Sult2a1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SULT2A1 CRISPR/Cas9 KO Plasmid (m) and SULT2A1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sult2a1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SULT2A1 HDR Plasmid (m) and SULT2A1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sult2a1 homology arms to support homology-directed repair at defined Sult2a1 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.