The HIVEP1 Knockout HAP1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout population targeting HIVEP1 in the HAP1 human cell line. This pool provides a loss-of-function model to study HIVEP1, a zinc finger transcription factor involved in immune regulation and apoptosis. The polyclonal format includes heterogeneous mutations, avoiding clonal artifacts and enabling robust population-level assays.
HAP1 is a near-haploid cell line derived from KBM-7, originating from a male patient with chronic myeloid leukemia in blast crisis. Its haploid genotype simplifies genetic studies by eliminating diploid compensation, and it retains signaling pathways relevant to hematopoietic malignancies. HAP1 cells are widely employed in functional genomics and drug discovery because of their ease of culture and the unambiguous genotype?Cphenotype relationships afforded by haploidy.
HIVEP1 encodes a zinc finger protein that binds NF-??B-like enhancer sequences, functioning as a transcriptional regulator activated by TNF-?? and IL-1??. It acts downstream of T-cell receptor and interferon signaling and interacts with NF-??B p65, p50, and I??B??. HIVEP1 controls expression of downstream targets including c-MYC, MHC class I genes, CCL5, IL-2, and apoptosis-related genes, thereby modulating NF-??B-mediated immune responses and cell survival.
In HAP1 cells, which depend on BCR-ABL signaling, HIVEP1 knockout likely disrupts NF-??B-dependent transcription and apoptotic thresholds, affecting imatinib sensitivity and stress responses. Disruption of HIVEP1 may derepress certain NF-??B target genes or alter the balance between pro-survival and pro-apoptotic signals, providing a platform to explore transcription factor cooperativity. The near-haploid background amplifies phenotypic effects, making it suitable for studying connections between immune transcription factors and leukemic drug resistance using Annexin V apoptosis and imatinib viability assays.
Applications include NF-??B pathway interrogation via luciferase reporters and ChIP-qPCR, target gene quantification by RT-qPCR for c-MYC and cytokine mRNAs, apoptosis and cell cycle analysis, and drug resistance screening. This model supports functional transcription factor research, leukemia biology, and immune modulation studies. Standard characterization includes western blotting for HIVEP1 and NF-??B subunits. For technical details or ordering, please contact Ascent Research.