The BPNT1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma epithelial cell line (Homo sapiens). This product provides a loss-of-function model for the BPNT1 gene, which encodes a bisphosphate nucleotidase. The polyclonal knockout population offers a heterogeneous pool of gene-disrupted cells, well-suited for pooled functional genomics and pharmacological studies without requiring clonal isolation. CRISPR/Cas9-mediated gene disruption efficiently targets the endogenous locus, generating a versatile tool for investigating BPNT1-dependent processes in a widely utilized cancer cell line.
HeLa cells are an immortalized epithelial line originally derived from a cervical adenocarcinoma and are distinguished by their HPV18-positive status. Extensively characterized across signal transduction, cancer biology, and drug screening applications, these cells provide a robust and defined platform for mechanistic studies. Their transformed epithelial background and rapid proliferation make them particularly relevant for dissecting BPNT1 functions linked to metabolic regulation, oncogenic signaling, and stress responses.
BPNT1 encodes an evolutionarily conserved bisphosphate nucleotidase that hydrolyzes 3??-phosphoadenosine 5??-phosphate (PAP) to AMP and inositol 1,4-bisphosphate to inositol monophosphate, integrating sulfate metabolism with phosphatidylinositol signaling. The enzyme is potently inhibited by lithium, placing it at a critical node in lithium-sensitive pathways. BPNT1 functions downstream of intracellular inositol levels and upstream of AMP and inositol monophosphate production, influencing phosphatidylinositide turnover through interactions with PAP and inositol 1,4-bisphosphate. Its activity modulates key signaling components, including IMPA1, IMPA2, PI3K, and PLC, such that BPNT1 knockout disrupts inositol phosphate balance and sulfur donor availability.
In the HeLa cell context, BPNT1 knockout impairs canonical PAP and inositol bisphosphate degradation, leading to substrate accumulation and altered downstream metabolite profiles. This perturbation is expected to shift lithium sensitivity and phosphatidylinositol signaling dynamics, offering a cellular model to dissect the molecular basis of lithium action and toxicity. The HeLa background, with active nucleotide and inositol metabolism, facilitates exploration of compensatory mechanisms and oncogenic dependencies. The model therefore informs research into bipolar disorder, neurodevelopmental disorders, and cervical cancer biology where lithium pharmacodynamics and phosphoinositide dysregulation are clinically relevant.
Typical applications for the BPNT1 Knockout HeLa Polyclonal Cells include expression analysis by western blotting and RT-qPCR, subcellular localization via immunofluorescence, enzymatic phosphatase activity assays, and lithium sensitivity profiling. Advanced uses encompass inositol phosphate profiling by mass spectrometry, transcriptome-wide analysis via RNA-seq, and phenotypic screening with flow cytometry. The knockout population is suited for drug target validation, signaling crosstalk studies, and interrogating sulfur metabolism and phosphoinositide pathway interactions. For further details or custom inquiries, please contact Ascent Research.
