SULT1C2 CRISPR/Cas9 KO Plasmid (h): sc-406300
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SULT1C2 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 SULT1C2 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 | |
SULT1C2 CRISPR/Cas9 KO Plasmid (h) | sc-406300 | 20 µg | $397.00 |
Overview
SULT1C2 encodes a cytosolic sulfotransferase that catalyzes the transfer of sulfate from 3′-phosphoadenosine-5′-phosphosulfate (PAPS) to hydroxyl- and amine-containing substrates, increasing their polarity and modulating bioavailability. As part of phase II metabolism, SULT1C2 participates in xenobiotic and endobiotic biotransformation processes that influence cellular handling of hormones, environmental chemicals, and dietary compounds. Its activity interfaces with broader detoxification networks and can shape metabolite profiles that impact oxidative stress responses and signaling tone. Altered sulfation capacity has been linked to inter-individual differences in chemical susceptibility and has been explored in the context of carcinogen metabolism and toxicology-relevant phenotypes.
SULT1C2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SULT1C2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SULT1C2 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 SULT1C2 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 SULT1C2 protein expression.
This CRISPR knockout system enables efficient generation of SULT1C2-deficient cell models for investigation of SULT1C2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SULT1C2 exon(s) critical for SULT1C2 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 SULT1C2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SULT1C2 CRISPR/Cas9 KO Plasmid (h) and SULT1C2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SULT1C2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SULT1C2 HDR Plasmid (h) and SULT1C2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SULT1C2 homology arms to support homology-directed repair at defined SULT1C2 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.