HS3ST4 CRISPR/Cas9 KO Plasmid (h): sc-408176
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HS3ST4 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 HS3ST4 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 | |
HS3ST4 CRISPR/Cas9 KO Plasmid (h) | sc-408176 | 20 µg | $397.00 |
Overview
HS3ST4 encodes heparan sulfate-glucosamine 3-O-sulfotransferase 4, a Golgi-resident enzyme that catalyzes 3-O-sulfation during heparan sulfate proteoglycan (HSPG) biosynthesis. This late-stage modification helps define heparan sulfate fine structure and modulates binding of extracellular ligands, shaping signaling pathways such as FGF, VEGF, WNT, and chemokine-guided processes that influence adhesion, migration, and differentiation. By altering HSPG-dependent receptor–ligand interactions and extracellular matrix organization, HS3ST4 can affect cell–cell communication and microenvironmental cues relevant to developmental programs and tumor-associated phenotypes. Dysregulated heparan sulfate sulfation patterns, including changes in 3-O-sulfation capacity, are frequently examined in studies of cancer biology, inflammation, and tissue remodeling.
HS3ST4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the HS3ST4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the HS3ST4 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 HS3ST4 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 HS3ST4 protein expression.
This CRISPR knockout system enables efficient generation of HS3ST4-deficient cell models for investigation of HS3ST4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting HS3ST4 exon(s) critical for HS3ST4 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 HS3ST4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by HS3ST4 CRISPR/Cas9 KO Plasmid (h) and HS3ST4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the HS3ST4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by HS3ST4 HDR Plasmid (h) and HS3ST4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by HS3ST4 homology arms to support homology-directed repair at defined HS3ST4 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.