The HSPBP1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HeLa cells with targeted disruption of the HSPBP1 gene. This heterogeneous loss-of-function model avoids clonal selection, providing a population-level tool for functional studies and minimizing clone-specific biases. Cells are ready for immediate use in a variety of downstream assays, enabling robust and reproducible investigation of HSPBP1 function.
HeLa cells are an HPV18-positive human cervical adenocarcinoma cell line, widely employed as a tumorigenic model for cervical cancer research. Their immortalized nature and stable growth characteristics support reproducible gene editing, while the viral oncoprotein background facilitates studies of chaperone interactions in the context of HPV-mediated oncogenesis.
HSPBP1 functions as a co-chaperone that binds and inhibits HSP70 (HSPA1A) ATPase activity, negatively regulating protein folding and anti-apoptotic functions. Upstream, it is induced by HSF1 under heat shock and oxidative stress, operating within complexes containing HSP90, STIP1, and STUB1. Downstream, HSPBP1 influences the stability of HSP70 client proteins and apoptosis regulators such as BCL2, BAX, and caspase-3 (CASP3). Knockout of HSPBP1 is predicted to enhance HSP70 activity, altering stress-induced apoptosis signaling through pathways involving DNAJB1 and HSP90AA1.
In HeLa cells, where apoptosis is dysregulated due to HPV18 E6 expression, HSPBP1 knockout provides a unique model to examine how HSP70 activity modulation impacts protein homeostasis and cell survival. This system can be exploited to study the role of the HSP70-HSPBP1 axis in stress resilience and drug sensitivity in cervical adenocarcinoma, offering a platform to explore co-chaperone-dependent regulatory mechanisms and therapeutic targeting of the HSP70 machinery.
Applications include mechanistic studies of HSP70 chaperone regulation, apoptosis signaling in cancer, cellular stress response assays, and identification of HSP70 client proteins. Typical assays performed with these cells encompass Western blotting, apoptosis flow cytometry, co-immunoprecipitation of HSP70, RT-qPCR for heat shock genes, and clonogenic survival analysis. This model supports cancer therapeutic target validation and stress biology research. For additional information, please contact Ascent Research.
