The EGR3 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the EGR3 gene. Generated from the HAP1 cell line, this product consists of a pooled population of cells carrying diverse gene-disrupting edits, providing a robust and heterogeneous model that avoids clonal artifacts. It is immediately suitable for functional genomics, pathway analysis, and drug target validation experiments.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line, exhibiting a predominantly haploid karyotype with disomy for chromosome 8. This genetic simplicity enables efficient CRISPR/Cas9-mediated gene disruption by targeting a single allele, making HAP1 a preferred platform for genetic screens and functional assays. The adherent cells grow robustly and retain key signaling pathways relevant to cancer and immune research.
EGR3 encodes a zinc-finger transcription factor rapidly induced by nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) via the TrkA?CRas?CRaf?CMEK?CERK signaling cascade. Phosphorylated ERK promotes EGR3 expression, and the protein binds GC-rich DNA elements to regulate target genes, including the pro-apoptotic FASLG and angiogenic VEGFA. Transcriptional activity is modulated by corepressors NAB1 and NAB2, and EGR3 also interacts with coactivators CBP/p300 and transcription factors Sp1 and NF-??B. These interactions control apoptosis, angiogenesis, neuronal development, and cell cycle progression, linking EGR3 to genes such as CDKN1A (p21) and TP53.
In the HAP1 background, EGR3 knockout offers unambiguous functional insights due to the near-haploid state, eliminating allelic complexity. This model is particularly relevant for dissecting EGR3??s roles in leukemia and other cancers, as well as in NGF/BDNF-dependent neuronal and immune signaling. The polyclonal population mirrors biological heterogeneity, enabling studies of EGR3 loss in diverse cellular contexts.
Recommended applications include Western blot validation of EGR3 disruption, RT-qPCR analysis of FASLG and VEGFA expression, apoptosis assays using Annexin V, and VEGF ELISA for angiogenic output. NGF-induced phospho-ERK assays can probe signaling dependencies, while RNA-sequencing enables genome-wide transcriptomic profiling. These cells are valuable for functional genomics screens, drug target validation, and pathway dissection in neurobiology, oncology, and immunology. For technical inquiries, please contact Ascent Research.
