The ANKRD54 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from HeLa cells, with targeted disruption of the ANKRD54 gene to create a loss-of-function model for studying Src family kinase signaling. This polyclonal format provides a heterogeneous pool of gene-edited cells, avoiding clonal artifacts and enabling robust experimental reproducibility. Derived from the widely used HeLa cervical adenocarcinoma line, these cells are ideal for investigating ANKRD54 function in epithelial cancer contexts.
The host HeLa cell line is an immortalized human cervical adenocarcinoma epithelial line originally derived from Henrietta Lacks. These cells are a cornerstone of biomedical research, known for their fast proliferation, aneuploidy, and expression of HPV18 E6/E7 oncoproteins that inactivate p53 and Rb. This genetic background makes HeLa cells a pertinent model for cervical cancer biology and the interplay between viral oncogenesis and host signaling pathways.
ANKRD54 encodes an ankyrin repeat protein that scaffolds and inhibits Lyn kinase, a member of the Src family, via SH3 domain binding. This curtails Lyn-mediated activation of Syk, PI3K/AKT, ERK1/2 MAP kinase, and NF-??B pathways, which are normally induced by B-cell receptor or IL-4 stimulation. ANKRD54 additionally associates with Fyn and Src, thereby integrating upstream signals to modulate cellular proliferation and survival.
In HeLa cells, ANKRD54 knockout may perturb Lyn/Src-dependent regulation of epithelial growth and cytokine production. Given that HeLa cells express HPV18 E6/E7, which constitutively activate proliferative pathways, loss of ANKRD54-mediated inhibition can further enhance PI3K/AKT and MAPK signaling. This may lead to altered proliferation rates, resistance to apoptosis, and amplified inflammatory signals, making the model valuable for dissecting how Src family kinase control influences cervical cancer progression and for testing the tumor-suppressive capacity of ANKRD54.
Applications include mechanistic investigation of Lyn/Src signaling in cervical cancer, screening of Lyn kinase inhibitors, and studies of B-cell receptor and autoimmune pathways. Typical assays involve western blotting for phospho-Lyn (Tyr507) and downstream effectors AKT and ERK1/2, co-immunoprecipitation of ANKRD54 with Lyn, NF-??B luciferase reporter assays, MTT/BrdU proliferation tests, and Annexin V apoptosis analyses. The cells also support Src kinase activity measurements and phospho-signaling arrays. For further details or to request a quotation, please contact Ascent Research.
