The AMOT Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-generated polyclonal knockout cell population derived from the HeLa human cervical carcinoma epithelial cell line. This model disrupts the AMOT gene, which encodes angiomotin, a scaffolding protein central to cell migration, polarity, and angiogenesis. The polyclonal format ensures population-level heterogeneity and avoids artifacts that can arise from single clones, making it suitable for robust loss-of-function investigations across multiple experimental replicates. This KO product provides a versatile tool for studying AMOT-dependent phenotypes in cancer biology and signal transduction.
HeLa cells are an immortalized human cervical carcinoma epithelial line originally established from an adenocarcinoma, serving as a primary model in cancer biology and virology. Their rapid proliferation, well-characterized signaling networks, and HPV-positive status make them particularly valuable for studying pathways that control cell growth and motility. In HeLa cells, AMOT localizes to tight junctions and the cortical actin cytoskeleton, where it scaffolds interactions crucial for regulating YAP/TAZ subcellular distribution.
Angiomotin functions as a scaffold that directly binds YAP and TAZ transcriptional co-activators, tethering them to tight junction complexes or the actin cytoskeleton. This sequestration prevents their nuclear translocation and inhibits TEAD1-4-dependent transcription of genes promoting proliferation and migration. AMOT is phosphorylated by LATS1/2 kinases??core components of the Hippo pathway??and is influenced by RhoA-mediated actin dynamics. Outside the Hippo axis, AMOT interacts with angiostatin and Merlin (NF2) to regulate endothelial cell migration and angiogenesis. At tight junctions, AMOT associates with proteins such as ZO-1, linking cell polarity to growth signaling.
Knockout of AMOT in HeLa cells allows researchers to study how loss of junctional tethering affects YAP/TAZ nuclear accumulation and transcriptional activity, with implications for epithelial-mesenchymal transition, invasion, and loss of contact inhibition. This model is particularly relevant for cervical cancer research, as HeLa??s HPV oncoproteins may intersect with AMOT-dependent pathways. Functional assays such as wound healing and transwell migration can reveal AMOT??s role in cell motility, while immunofluorescence can visualize changes in tight junction integrity and actin organization.
This polyclonal KO product supports a broad range of applications: Western blotting for AMOT and phospho-YAP, co-immunoprecipitation of AMOT-YAP complexes, and YAP/TAZ-responsive luciferase reporter assays. Functional analyses include wound-healing migration, transwell invasion, and endothelial tube formation to probe angiogenesis. The model is also applicable in drug screens targeting AMOT interactions and in mechanotransduction experiments assessing how force regulates YAP/TAZ. For more information, please contact Ascent Research.
