The DLGAP4 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HAP1 cell line, in which the DLGAP4 gene has been disrupted. This knockout product delivers a heterogeneous pool of cells, each carrying distinct loss-of-function mutations at the target locus, providing a robust model for studying DLGAP4 function without clonal selection.
HAP1 is a human near-haploid chronic myeloid leukemia (CML) cell line with fibroblast-like morphology. Its near-haploid genome (only one copy of most chromosomes) greatly facilitates CRISPR/Cas9-mediated gene knockout by reducing target allele number and minimizing genetic redundancy. Widely used in functional genomics, HAP1 offers a genetically stable and easily transfectable system for dissecting gene function in a simplified cellular background.
DLGAP4 encodes a postsynaptic density scaffolding protein that anchors PSD-95 (DLG4) at the membrane, promoting the clustering of NMDA receptors (containing GRIN2B subunits) and AMPA receptors (GRIA1). Through its interactions with PSD-95, Shank proteins, and GKAP family members, DLGAP4 organizes a multiprotein complex essential for glutamatergic synapse organization and synaptic plasticity. Additional pathway components linked to this network include CAMK2, SHANK1, HOMER1, and SynGAP1. Loss of DLGAP4 disrupts receptor anchoring and downstream signaling, impairing synaptic transmission.
Within HAP1 cells, DLGAP4 knockout provides a tractable model for examining the protein??s biochemical interactions and stability outside the neuronal context. The haploid background ensures that even single-allele disruptions result in complete loss of function, yielding clear phenotypes in protein interaction studies. The polyclonal composition mirrors naturally variable knockout populations, making it ideal for pooled screens, proteomic analyses, and studying gene dosage effects.
This knockout model is applicable to functional genomics, drug target validation, and mechanistic studies of synaptic signaling pathways. Typical assays include Western blotting and RT-qPCR for knockout confirmation, co-immunoprecipitation to assess binding to PSD-95 and Shank proteins, and immunofluorescence for subcellular localization. The cells are also amenable to proteomics and protein interaction assays to map altered signaling networks. In neuropsychiatric research, the model aids in exploring molecular underpinnings of schizophrenia, autism spectrum disorder, and intellectual disability. For further information or technical support, please contact Ascent Research.
