The DYRK3 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from HeLa cells, featuring targeted disruption of the DYRK3 gene. This polyclonal knockout model provides a heterogeneous pool of gene-edited cells, enabling robust loss-of-function studies without the biases of single-cell clonal selection. The CRISPR/Cas9-mediated gene disruption eliminates DYRK3 protein expression, facilitating investigation of its cellular functions across a diverse genetic background.
The host HeLa cell line is a human cervical adenocarcinoma-derived epithelial cell line, established in 1951 and widely employed in cancer biology, drug screening, and signal transduction research. As an HPV18-positive immortalized cell line, HeLa cells exhibit rapid proliferation and well-characterized signaling networks, making them a versatile platform for studying oncogenic processes and therapeutic responses.
DYRK3 encodes a dual-specificity tyrosine-regulated kinase that integrates nutrient and stress signals to control cell growth and survival. DYRK3 phosphorylates downstream substrates such as AKT1S1 (PRAS40) and CYFIP1, thereby promoting mTORC1 signaling and inhibiting autophagy. It responds to upstream cues including insulin/IGF-1 and EGF, as well as osmotic and oxidative stress. Through interactions with HSP90, CDC37, CRMP4, and G3BP1, DYRK3 also governs stress granule dynamics, linking environmental conditions to translational control and apoptosis regulation.
In the HeLa cellular context, DYRK3 knockout disrupts key oncogenic and stress-response pathways. Loss of DYRK3 is expected to attenuate mTORC1 activity, reduce proliferation, and enhance susceptibility to apoptosis, while altering stress granule assembly and autophagy flux. These changes are particularly relevant for modeling cancer cell dependencies and for evaluating DYRK3 as a therapeutic target in malignancies such as glioblastoma and acute myeloid leukemia. The epithelial origin of HeLa cells also supports studies of DYRK3 in carcinoma biology.
Researchers can employ this polyclonal knockout cell population in a variety of assays, including western blotting for DYRK3 and phospho-PRAS40, immunofluorescence analysis of stress granules, autophagy flux measurements, cell proliferation and colony formation assays, and apoptosis detection. The model is well-suited for functional validation of DYRK3 in mTOR signaling, stress granule biology, and drug target discovery. For additional information or to initiate a collaboration, please contact Ascent Research.
