The CD37 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the CD37 gene. This product consists of a heterogeneous pool of HAP1 cells carrying targeted gene disruptions at the CD37 locus, resulting in functional ablation of the encoded tetraspanin protein. The polyclonal format captures a diversity of editing outcomes, making it a robust model for studying gene function in a population context without clonal selection biases.
The host cell line, HAP1, is a near-haploid human cell line derived from the male chronic myeloid leukemia cell line KBM-7. Its near-haploid karyotype simplifies genetic manipulation and interpretation of knockout phenotypes by eliminating heterozygous masking. HAP1 cells are widely employed in functional genomic screens and CRISPR-based perturbation studies, offering a versatile and scalable platform for mechanistic dissection of gene function across biological processes.
CD37 belongs to the tetraspanin superfamily and organizes membrane microdomains that regulate B-cell receptor (BCR) signaling and integrin-mediated adhesion. CD37 forms complexes with other tetraspanins such as CD81, CD82, and CD9, and interacts with integrins (e.g., ITGAL/ITGB2), MHC class II molecules, and the CD19/CD21 co-receptor complex. Upon BCR engagement, CD37 facilitates signal propagation to downstream kinases including SYK, LYN, and PI3K, which in turn activate MAPK/ERK and AKT pathways. CD37 function is also influenced by IL-4 stimulation and is essential for immune synapse formation and B-cell adhesion.
In the HAP1 haploid background, knockout of CD37 disrupts tetraspanin web assembly and alters downstream signaling, enabling clear genotype-phenotype correlations. The absence of a second allele ensures that each editing event unequivocally abrogates gene function, providing a definitive loss-of-function model. This cellular context is particularly advantageous for high-throughput genetic screens and for studying CD37-dependent molecular interactions without diploid genetic compensation. It also facilitates identification of synthetic lethal interactions and other CD37-related dependencies.
Researchers can employ these polyclonal knockout cells to investigate B-cell signaling mechanisms, tetraspanin-mediated adhesion in immune synapses, and CD37 as a therapeutic target in B-cell malignancies such as non-Hodgkin lymphoma and chronic lymphocytic leukemia. Appropriate assays include flow cytometry to confirm loss of surface CD37, western blotting for phospho-SYK and phospho-LYN, co-immunoprecipitation of CD37-interacting partners, migration assays on integrin ligands, and RNA sequencing to profile BCR pathway gene expression. This model also supports functional genomic screens exploiting the haploid system. For further details, please contact Ascent Research.
