The BPNT1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population in which the BPNT1 gene has been disrupted. This product provides a genetically heterogeneous pool of knockout cells, enabling robust loss-of-function studies without clonal isolation. The polyclonal format preserves population-level diversity while eliminating functional BPNT1 expression, making it suitable for pooled screening and comparative analyses against wild-type controls. These cells retain the parental HAP1 background??s suitability for high-throughput genetic and pharmacological investigations.
The host HAP1 cell line is a near-haploid human myeloid leukemia model derived from KBM-7 chronic myeloid leukemia cells. HAP1 cells are male, adherent, and possess a near-haploid karyotype except for disomy of chromosome 8. This unique ploidy simplifies gene editing and facilitates unambiguous interpretation of knockout phenotypes, as most genes are present in only one copy. Originally established for haploid genetic screening, HAP1 cells are widely employed in functional genomics, drug discovery, and mechanistic signaling studies. Their myeloid leukemia origin further adds relevance to hematological malignancy research.
BPNT1 encodes a bisphosphate 3′-nucleotidase that dephosphorylates PAP and PAPS to AMP. Its activity depends on Mg2? and is inhibited by lithium. By producing AMP, BPNT1 stimulates AMPK signaling and influences mTOR pathway activity. Hydrolysis of PAP/PAPS also prevents feedback inhibition of sulfotransferases, sustaining sulfur metabolism. Loss of BPNT1 disrupts inositol phosphate metabolism, altering levels of metabolites such as inositol 1,3,4-trisphosphate and inositol 1,4-bisphosphate. BPNT1 thus integrates lithium responsiveness, energy homeostasis, and phosphoinositide signaling.
In the HAP1 background, BPNT1 knockout affords a straightforward model to investigate how loss of this phosphatase affects cellular lithium sensitivity and inositol phosphate dynamics. The haploid genomic environment eliminates confounding effects from a second allele, ensuring that observed phenotypes directly reflect BPNT1 disruption. This model is particularly valuable for dissecting the mechanistic links between lithium??s therapeutic actions in bipolar disorder and its interference with inositol recycling, as well as for exploring the role of sulfation imbalance in skeletal dysplasias. The myeloid leukemia context also permits examination of BPNT1??s potential involvement in hematological pathogenesis, though its primary utility lies in signaling network analysis.
BPNT1 Knockout HAP1 Polyclonal Cells support diverse research applications such as CRISPR knockout screening, lithium response mechanism studies, inositol phosphate signaling profiling, and sulfation pathway analysis. Common assays include Western blotting for BPNT1 and phospho-AMPK, PAP/PAPS phosphatase activity assays, lithium sensitivity growth tests, AMP/ATP ratio quantification, inositol phosphate mass spectrometry, and sulfotransferase activity measurements. These cells may further be employed in pooled genetic modifier screens to dissect BPNT1-related networks. For more information, please contact Ascent Research.
