The KRT8 Knockout HeLa Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal HeLa cell population with targeted disruption of the human KRT8 gene, creating a loss-of-function model for keratin 8. As a polyclonal population, it contains diverse edited alleles and is not derived from a single clone, providing a robust system for studying gene function without clonal selection bias. This format is well suited for applications where gene inactivation is needed across a heterogeneous cell pool, such as in pooled screening or functional assays in an epithelial carcinoma background.
HeLa cells are an adherent, aneuploid cervical epithelial carcinoma line originally derived from a human adenocarcinoma in 1951. They harbor HPV-18 DNA and express viral oncoproteins E6 and E7, which contribute to their transformed state and deregulated cell cycle. As a canonical model for cervical cancer, HeLa cells are routinely employed to study oncogenic signaling, cytoskeletal dynamics, and drug responses.
Keratin 8 is a type II intermediate filament protein that forms obligate heterodimers with keratin 18 (KRT18) to assemble the keratin filament network, conferring mechanical resilience and structural integrity to epithelial cells. In addition to its cytoskeletal function, KRT8 serves as a signaling scaffold through direct interactions with 14-3-3 proteins, TNFR2, SRC kinase, and PKC epsilon. Its activity is regulated by upstream factors such as p63, AP-1, and ERK1/2, and it modulates downstream targets including NF-??B, AKT, and Bcl-2 family proteins, thereby linking filament organization to apoptotic and stress signaling pathways.
In the HeLa cervical cancer context, disruption of KRT8 destabilizes the keratin network, altering cell mechanics and potentially affecting migration, invasion, and sensitivity to chemotherapeutics. Because HeLa cells natively express KRT8/KRT18 heterodimers, this knockout provides a relevant model to examine how keratin filament collapse influences epithelial-to-mesenchymal transition and metastatic traits in an HPV-positive carcinoma. It also allows dissection of KRT8??s non-structural signaling roles, including its impact on NF-??B and AKT pathways.
Researchers can apply this polyclonal knockout population in a variety of assays: Western blotting to verify KRT8 protein ablation, immunofluorescence and phalloidin staining to visualize cytoskeletal reorganization, wound healing and transwell invasion assays to quantify cell motility, flow cytometry with Annexin V/PI to measure apoptosis, co-immunoprecipitation to probe KRT8/KRT18 heterodimer integrity, and luciferase reporter assays for NF-??B transcriptional activity. These tools enable detailed investigation of the interplay between intermediate filament integrity, stress kinases, and apoptotic regulators in epithelial cancer biology. For pricing, technical specifications, and ordering inquiries, please contact Ascent Research.
