The AJUBA Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the AJUBA gene. This product provides a heterogeneous pool of HeLa cells carrying targeted disruption of AJUBA, avoiding clonal artifacts and enabling robust analysis of AJUBA-dependent pathways. The polyclonal knockout model is generated using CRISPR/Cas9-mediated gene disruption, ensuring effective abrogation of AJUBA protein expression across the population.
The host cell line, HeLa, is an immortalized epithelial cell line derived from a cervical adenocarcinoma (Henrietta Lacks, 1951). HeLa cells are among the most widely used human cell lines in biomedical research, characterized by rapid proliferation, ease of culture, and a well-annotated genomic landscape. They retain key epithelial features such as adherens junctions and actin cytoskeletal networks, making them an appropriate model for studying cell adhesion, migration, and signaling processes relevant to cervical cancer biology.
AJUBA encodes a LIM domain scaffold protein that localizes to adherens junctions and interacts with E-cadherin, alpha-catenin, beta-catenin, and actin filaments. Functionally, AJUBA inhibits LATS1/2 kinase-mediated phosphorylation of YAP/TAZ, thereby promoting YAP/TAZ nuclear translocation and TEAD-dependent transcription. This process is modulated by upstream signals such as cell-cell contact inhibition and mechanical strain. By relieving YAP/TAZ from LATS-dependent suppression, AJUBA facilitates expression of downstream targets including CTGF, CYR61, and ANKRD1, which drive cell proliferation and migration. Thus, AJUBA acts as a critical regulator at the intersection of the Hippo pathway and actin cytoskeleton dynamics.
In HeLa cells, endogenous AJUBA contributes to the oncogenic potential by sustaining YAP/TAZ activity and supporting anchorage-independent growth. AJUBA knockout disrupts this signaling axis, offering a physiologically relevant model to investigate how loss of AJUBA affects cervical adenocarcinoma progression. Researchers can assess changes in YAP nuclear localization, target gene expression, and functional phenotypes such as reduced migration and invasion. This model is particularly suited to explore the crosstalk between cell adhesion complexes and Hippo signaling in an epithelial cancer background.
This polyclonal knockout cell product is applicable in diverse experimental workflows, including western blotting for AJUBA, YAP/TAZ, and phospho-YAP; immunofluorescence imaging of YAP subcellular distribution; and cell migration/proliferation assays. RT-qPCR can be used to quantify CTGF and CYR61 transcript levels, while TEAD luciferase reporter assays measure Hippo pathway transcriptional output. These cells are valuable for studies on tumor invasion and metastasis, as well as for screening therapeutic agents that target AJUBA-interacting proteins. For additional technical information, please contact Ascent Research.
