The IKZF5 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the near-haploid HAP1 cell line, targeting the IKZF5 gene which encodes a zinc finger transcription factor of the Ikaros family. This product provides a heterogeneous pool of cells with diverse loss-of-function mutations introduced by CRISPR/Cas9-mediated gene disruption, facilitating robust functional genomics studies without the bias of clonal selection.
HAP1 cells are a male-derived, near-haploid cell line originally established from the KBM-7 chronic myeloid leukemia line. Their haploid genomic background enables high-efficiency gene targeting, making them an ideal host for knockout screens and systematic genetic perturbation. As a hematopoietic cell model, HAP1 retains key regulatory networks relevant to blood cell development and malignancy, providing a physiologically meaningful context for studying transcriptional regulators of hematopoiesis.
IKZF5 functions downstream of IL-7 receptor stimulation and Notch signaling, and integrates cues from pre-B cell receptor signaling to orchestrate B-cell lineage commitment and differentiation. It transcriptionally promotes expression of critical effectors such as CD79A and the recombinase genes RAG1 and RAG2, and interacts with other Ikaros family members (IKZF1, IKZF3) as well as the NuRD complex and histone deacetylases to modulate chromatin remodeling and gene silencing. Disruption of IKZF5 in HAP1 cells thus perturbs transcriptional networks controlling immunoglobulin gene rearrangement and B-cell maturation, directly affecting B-cell receptor signaling and hematopoietic lineage specification.
Given the hematopoietic origin of HAP1, this knockout model offers a powerful system to investigate how loss of IKZF5 alters lymphopoiesis and contributes to malignancies such as B-cell acute lymphoblastic leukemia and B-cell lymphoma. The polyclonal population allows assessment of heterogeneous cellular responses, avoiding artifacts from clone-specific adaptations, and is well-suited for pooled screening approaches including drug sensitivity and proliferation assays to uncover IKZF5-dependent vulnerabilities.
Researchers can employ this model in diverse experimental workflows, including RNA-seq and ChIP-seq to map transcriptomic and epigenomic changes, flow cytometry to monitor B-cell marker expression, and western blotting or RT-qPCR to validate downstream targets. The cells are suitable for functional assays such as proliferation analysis, drug sensitivity profiling, and genetic interaction studies, making them a versatile tool for dissecting IKZF5-mediated regulatory circuits in hematopoiesis and lymphoid malignancies. For additional information, please contact Ascent Research.
