The GFAP Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the GFAP gene in HeLa cells. This heterogeneous pool contains various loss-of-function mutations, avoiding clonal artifacts and enabling robust population-level analyses of GFAP deficiency.
The HeLa cell line is an immortalized human cervical adenocarcinoma epithelial line, aneuploid and HPV18-positive, with adherent morphology. Widely used in biomedical research, HeLa cells provide a well-characterized model for cancer biology, cytoskeletal dynamics, and cytokine signaling, offering a non-astrocytic context for studying GFAP.
GFAP is a type III intermediate filament protein primarily expressed in astrocytes, where it maintains structure, motility, and response to injury. Its transcription is driven by STAT3 downstream of CNTF, LIF, and IL-6 via the gp130-JAK1/2 pathway, and is also regulated by NF-??B and Notch. GFAP interacts with vimentin, nestin, and plectin to organize the cytoskeleton, and its loss disrupts cell migration and stress responses.
In HeLa cells, which lack endogenous GFAP, knockout allows dissection of non-astrocytic GFAP functions, such as roles in epithelial cell migration and cytokine responsiveness. Disruption of GFAP impairs cytoskeletal integrity and may alter pathways implicated in cancer invasiveness. The model can be used to study disease-associated mutations, like those in Alexander disease, through complementation experiments.
Applications include functional analysis of cell migration and cytoskeleton using immunofluorescence and migration assays; studying STAT3-mediated regulation with phospho-STAT3 ELISA and promoter-reporter assays; drug screening for intermediate filament modulators; and transcriptomic analysis via RNA-seq. Co-IP and Western blotting permit investigation of GFAP interactions with partners such as vimentin and ??B-crystallin. For further inquiries, please contact Ascent Research.
