The IBTK knockout HeLa polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the HeLa human cervical adenocarcinoma line. This product provides a heterogeneous pool of cells with targeted IBTK gene disruption, offering a loss-of-function model for studying the inhibitor of Bruton??s tyrosine kinase (IBTK). The polyclonal format maintains genetic diversity, suitable for robust functional assays without clonal bias. CRISPR/Cas9-mediated knockout yields a mixed population with IBTK inactivation ready for biochemical and pharmacological studies.
HeLa cells, an HPV18-immortalized epithelial line with inactivated p53 and Rb, are highly transfectable and widely used in research. Their rapid growth and extensive characterization make them a reliable host for gene editing. The epithelial origin allows investigation of IBTK in non-hematopoietic contexts relevant to solid tumors, including cervical, breast, and prostate cancers.
IBTK directly binds and inhibits BTK kinase activity, attenuating BCR-mediated signaling. This suppression reduces phosphorylation of downstream effectors PLC??2 and AKT, and inhibits NF-??B transcriptional activation, thereby modulating genes for survival, proliferation, and apoptosis. IBTK also interacts with PIN1, and its expression is regulated by BCR activation, cytokines, and NF-??B feedback. Thus, IBTK sits at a critical node controlling immune and oncogenic pathways.
In HeLa cells, IBTK knockout may perturb NF-??B signaling, altering proliferative and apoptotic thresholds already affected by HPV-driven oncogenesis. This model enables dissection of IBTK??s functions in a cancer cell background frequently used for studying solid tumors. It is valuable for investigating IBTK??s intersection with oncogenic networks and evaluating IBTK as a therapeutic target in malignancies with constitutive NF-??B activity.
Applications include BTK-signaling and NF-??B pathway analysis using luciferase reporters, western blotting for phospho-BTK, I??B??, and NF-??B subunits, and proliferation/apoptosis assays. Co-immunoprecipitation can examine IBTK-BTK or IBTK-PIN1 interactions in ectopic systems. The model supports drug target validation for BTK-related diseases and screening modulators of the IBTK-NF-??B axis in B-cell lymphomas, immunodeficiencies, and solid tumors. For details, contact Ascent Research.
