The HS3ST1 Knockout HeLa Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of HeLa cells with targeted disruption of the HS3ST1 gene. This population-based knockout model provides a heterogeneous pool of edited cells lacking functional HS3ST1 (heparan sulfate 3-O-sulfotransferase 1) expression, enabling loss-of-function studies without clonal isolation.
The host HeLa cell line is an HPV18-positive human cervical adenocarcinoma epithelial line originally derived from Henrietta Lacks. As one of the most widely utilized human cell lines in biomedical research, HeLa cells serve as a robust model for cancer biology, viral oncology, and cell signaling studies. Their rapid proliferation, ease of genetic manipulation, and well-characterized genomic landscape make them an ideal chassis for gene-editing applications.
HS3ST1 catalyzes the rate-limiting 3-O-sulfation of specific glucosamine residues within heparan sulfate proteoglycans, generating a unique pentasaccharide motif that binds and activates antithrombin III, a key serpin inhibitor of coagulation proteases such as thrombin and factor Xa. This modification is also essential for the formation of FGF2-FGFR signaling complexes and serves as an entry receptor for herpes simplex virus 1 (HSV-1) through interaction with glycoprotein D. The biosynthetic pathway involves sequential modifications by enzymes including NDST1, HS2ST1, and the copolymerases EXT1/EXT2, with HS3ST1 acting downstream. The sulfation reaction utilizes the cofactor PAPS, and its activity is influenced by upstream pathways such as Wnt and FGF signaling.
In the HeLa carcinoma context, HS3ST1-mediated heparan sulfate sulfation patterns may contribute to altered growth factor signaling, extracellular matrix interactions, and viral susceptibility. Loss of HS3ST1 is expected to reduce antithrombin binding capacity and perturb FGF2-FGFR-mediated proliferative signaling, potentially impacting cell growth and survival. This model thus offers a relevant system to dissect the role of 3-O-sulfated heparan sulfate in tumor progression, coagulation biology, and host-pathogen interactions within a cervical cancer background.
These polyclonal knockout cells are suitable for functional studies of heparan sulfate biosynthesis, coagulation cascade analysis, and HSV-1 entry mechanisms. Key assays include western blotting and RT-qPCR for gene disruption confirmation, immunofluorescence and mass spectrometry for sulfation patterning, antithrombin binding and coagulation assays (aPTT/PT) to probe cofactor activity, and FGF signaling reporter or viral entry assays to interrogate downstream effects. The population also supports drug screening for antithrombin modulators. For additional technical information, contact Ascent Research.
