The EGR4 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HAP1 cell line, offering targeted disruption of the EGR4 gene. This loss-of-function model enables investigation of EGR4’s role in signaling and tumor suppression without clonal isolation. The polyclonal format captures diverse editing events, providing a robust tool for functional genomics studies.
HAP1 is a near-haploid human cell line generated from the male KBM-7 chronic myeloid leukemia cell line. Its haploid karyotype simplifies genetic analysis and facilitates unambiguous genotype-phenotype correlations, making it a preferred model for CRISPR screens, drug sensitivity testing, and leukemic disease modeling.
EGR4 is a zinc-finger transcription factor that binds GC-rich motifs to regulate gene expression downstream of growth factor and stress stimuli. It is activated by EGF and NGF via the MAPK/ERK pathway, with MAPK1/3 (ERK1/2) mediating phosphorylation events. EGR4 is also transcriptionally regulated by p53 and interacts with corepressors NAB1 and NAB2 to fine-tune transcriptional programs. Key downstream targets include CDKN1A (p21) and BAX, which promote cell cycle arrest and apoptosis, linking EGR4 to tumor suppression and cellular stress responses.
In HAP1 leukemic cells, EGR4 knockout enables precise dissection of its tumor-suppressive functions. Loss of EGR4 can impair p53-mediated apoptosis and checkpoint control, revealing vulnerabilities in leukemia biology. The isogenic comparison between parental and knockout polyclonal cells allows quantification of EGR4-dependent effects on proliferation, drug sensitivity, and signal transduction, particularly within MAPK/ERK and p53 networks.
These cells support a range of applications, including Western blot-based confirmation of EGR4 disruption, RT-qPCR analysis of target gene expression (CDKN1A, BAX), cell proliferation and apoptosis assays, drug sensitivity profiling, and transcriptome-wide RNA-seq. The polyclonal design minimizes clonal bias, making it suitable for high-throughput functional genomics screens and validation studies. For further information, please contact Ascent Research.
