The CCDC90B Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HeLa cell line, designed for targeted disruption of the CCDC90B gene, also known as mitochondrial calcium uniporter regulator 1 (MCUR1). This product comprises a mixed cell pool harboring diverse genetic modifications at the CCDC90B locus, providing a versatile loss-of-function model to investigate its roles in human cervical adenocarcinoma cells.
The HeLa host cell line is an HPV18-positive cervical epithelial carcinoma cell line that has been extensively used in cancer research for decades. Its well-documented signaling networks, including perturbed calcium homeostasis, and robust growth properties make it a suitable platform for studying mitochondrial calcium dynamics and associated tumorigenic mechanisms.
CCDC90B functions as a scaffold subunit of the mitochondrial calcium uniporter (MCU) complex, mediating the uptake of Ca2+ into the mitochondrial matrix. Its activity is regulated by upstream signals including cytoplasmic Ca2+ elevation, the MICU1-MICU2 heterodimer, EMRE, and mitochondrial membrane potential. Within the complex, CCDC90B interacts directly with MCU, EMRE, MICU1, MICU2, and the inhibitory paralog MCUb. Once imported, mitochondrial Ca2+ activates key metabolic effectors such as pyruvate dehydrogenase and tricarboxylic acid (TCA) cycle enzymes, thereby stimulating ATP synthase and oxidative phosphorylation. Conversely, pathophysiological Ca2+ overload triggers opening of the mitochondrial permeability transition pore (mPTP), initiating apoptotic cell death. Thus, CCDC90B occupies a central node linking cytosol-to-mitochondria calcium signals to both bioenergetics and apoptosis.
In HeLa cervical carcinoma cells, disruption of CCDC90B expression abrogates efficient MCU-mediated calcium flux, rendering this knockout model invaluable for elucidating how mitochondrial calcium shuttling supports cancer cell metabolism, proliferation, and survival. HeLa cells depend on both glycolysis and oxidative phosphorylation, and CCDC90B-dependent Ca2+ uptake is critical for matching TCA cycle activity and ATP production to cellular energy demands. The knockout model enables direct assessment of how loss of this scaffold alters metabolic flux, sensitizes cells to calcium stress, and modulates apoptotic thresholds, providing insights into the metabolic adaptations and vulnerabilities of HPV-driven cancers.
These polyclonal knockout cells are suitable for a range of quantitative assays, including mitochondrial Ca2+ imaging with Rhod-2 AM, Seahorse XF metabolic flux profiling, ATP production measurements, annexin V/PI-based apoptosis detection, and MTT cell proliferation assays. They also facilitate immunoblotting and RT-qPCR to examine MCU complex assembly and expression. Drug screening studies targeting mitochondrial calcium pathways can employ this model to identify modulators of uniporter function. For further details or to inquire about custom solutions, please contact Ascent Research.
