AK7 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population originating from the HeLa human cervical adenocarcinoma line, with targeted disruption of the AK7 locus. This loss-of-function model enables investigation of adenylate kinase 7 function in a cancer epithelial context. The polyclonal format maintains population heterogeneity while providing stable heritable gene disruption, suitable for studies averaging phenotypic effects across a knockout pool or identifying subpopulations with distinct characteristics.
The HeLa host line is an immortalized human cervical adenocarcinoma cell line containing integrated HPV18 genome, with adherent morphology and robust proliferation. HeLa cells are extensively characterized and widely used for cell biology, virology, and cancer research. Their genetic tractability and well-mapped signaling and metabolic pathways make them an optimal platform for CRISPR-based functional genomics, ensuring relevance for dissecting tumor metabolism and nucleotide homeostasis.
AK7 encodes an adenylate kinase that catalyzes reversible phosphotransfer among adenine nucleotides, balancing ATP, ADP, and AMP pools. Transcription of AK7 is regulated by FOXJ1 and RFX transcription factors and is sensitive to the AMP/ATP ratio. AK7 functionally interacts with ATP, ADP, and AMP, and may act in concert with adenylate kinase isoforms AK1 and AK2. Downstream, AK7 activity influences ciliary beat frequency via dynein arm proteins DNAH5 and DNAI1, and sustains energy-dependent cellular processes. AK7 disruption therefore perturbs nucleotide interconversion and energy homeostasis, with implications for ciliary motility in relevant cell types and for broader metabolic signaling.
In HeLa cells, which lack motile cilia, AK7 knockout primarily impacts nucleotide metabolism. Impaired adenine nucleotide interconversion disrupts the ATP/ADP/AMP ratio, altering cellular energy charge and affecting ATP-dependent processes such as proliferation and stress adaptation. This model allows dissection of how adenylate kinase isoforms maintain energy balance in cancer cells and how metabolic imbalance interfaces with signaling pathways, including AMPK and other nucleotide sensors, providing insights into metabolic vulnerabilities of tumor cells.
Research applications include nucleotide metabolism and energy sensing studies, adenylate kinase functional analysis, and cancer cell metabolism investigation. Key assays are ATP/ADP ratio luminescence, Seahorse metabolic flux analysis, RT-qPCR, Western blotting, immunofluorescence, proliferation assays (MTT/CCK-8), and RNA-seq. The cells are suitable for drug screening targeting nucleotide pathways and for exploring compensatory mechanisms involving other adenylate kinases. For further information, contact Ascent Research.
