SULT1C4 CRISPR/Cas9 KO Plasmid (h): sc-417528
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SULT1C4 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 SULT1C4 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 | |
SULT1C4 CRISPR/Cas9 KO Plasmid (h) | sc-417528 | 20 µg | $397.00 |
Overview
SULT1C4 encodes a cytosolic sulfotransferase that catalyzes the transfer of sulfate from 3′-phosphoadenosine-5′-phosphosulfate (PAPS) to hydroxyl- and amine-containing substrates, generating sulfated metabolites with altered solubility and bioactivity. This phase II conjugation reaction contributes to xenobiotic detoxification and modulation of endogenous signaling molecules, intersecting with broader cellular networks controlling redox balance, hormone responsiveness, and metabolite clearance. Variation in sulfotransferase activity can influence the metabolic fate of environmental chemicals and pharmaceuticals, making SULT1C4 relevant to studies of inter-individual differences in chemical sensitivity and tissue-specific metabolism. Dysregulated sulfation capacity has also been linked in the literature to altered exposure biology and disease-associated metabolic phenotypes, supporting use of SULT1C4 as a functional node in metabolism-centered research.
SULT1C4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SULT1C4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SULT1C4 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 SULT1C4 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 SULT1C4 protein expression.
This CRISPR knockout system enables efficient generation of SULT1C4-deficient cell models for investigation of SULT1C4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SULT1C4 exon(s) critical for SULT1C4 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 SULT1C4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SULT1C4 CRISPR/Cas9 KO Plasmid (h) and SULT1C4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SULT1C4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SULT1C4 HDR Plasmid (h) and SULT1C4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SULT1C4 homology arms to support homology-directed repair at defined SULT1C4 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.