The CD38 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal population derived from human near-haploid HAP1 leukemia cells, engineered to abolish CD38 expression. This loss-of-function model enables precise dissection of CD38 biology in a robust polyclonal format, suitable for high-throughput functional genomics and drug discovery applications.
HAP1 cells originate from the KBM-7 chronic myelogenous leukemia line with a near-haploid karyotype that simplifies genome editing and facilitates clean knockout generation. Widely used in CRISPR screens and target validation, this immortalized leukemic background provides a genetically stable, highly transfectable platform for interrogating gene function in oncological and immunological contexts.
CD38 encodes a multifunctional ectoenzyme that synthesizes cyclic ADP-ribose (cADPR) from NAD+, mobilizing intracellular calcium via ryanodine receptors (RYR). Its expression is regulated by IL-2, TNF-alpha, retinoic acid, and NF-??B, and activated by T cell receptor signaling. Downstream, CD38 modulates calcium-sensitive effectors such as TRPM2 and sirtuins, and interacts with adhesion molecules PECAM-1 (CD31), CD16, LFA-1, and hyaluronan, promoting cell adhesion and signaling.
In the HAP1 leukemic context, CD38 disruption abrogates NAD+-dependent calcium signaling, enabling study of its role in malignant processes such as proliferation, adhesion, and drug resistance. The near-haploid genome ensures functional knockout, making the model highly relevant for hematologic malignancies like chronic lymphocytic leukemia and multiple myeloma, where CD38 is a validated therapeutic target.
Key applications include calcium flux assays to track cADPR-mediated signaling, flow cytometry for CD38 surface validation, and cell adhesion assays using CD31 or hyaluronan matrices. Drug sensitivity testing with anti-CD38 antibodies such as daratumumab supports preclinical evaluation of immunotherapies. These polyclonal knockout cells are compatible with large-scale genetic screens and biochemical pathway analysis. For further information, please contact Ascent Research.
