The EGR2 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the human EGR2 gene. This product features a heterogeneous pool of HAP1 cells carrying disruption of the EGR2 locus, enabling robust interrogation of EGR2-dependent signaling and transcriptional programs without clonal selection artifacts. The polyclonal format provides a biologically relevant population-level model that preserves genetic variability while abolishing EGR2 function, suitable for high-throughput functional genomics and pathway dissection.
The parental HAP1 cell line is a near-haploid human fibroblast-like cell line derived from the KBM-7 chronic myeloid leukemia isolate. Its haploid karyotype simplifies genetic manipulation and loss-of-function screens, as single-allele targeting can produce a null phenotype. HAP1 cells retain key signaling networks relevant to hematopoietic and neuronal lineages, making them a versatile platform for studying transcription factors like EGR2 that operate in multiple cell types.
EGR2 is a zinc finger transcription factor of the immediate-early gene family, activated downstream of MAPK/ERK signaling by stimuli such as EGF, NGF, IL-2, IL-4, and TCR engagement. Upon phosphorylation by ERK1/2, ELK1 and SRF promote EGR2 expression; EGR2 then transcriptionally regulates genes essential for peripheral nerve myelination (MPZ, PMP22, GJB1) and immune tolerance (FASL, p21Cip1). It interacts with corepressors NAB1/NAB2 and coactivators such as p300 and c-Jun, integrating signals from the TGF-?? pathway (TGFBR1/2, SMAD2/3) and T-cell receptor cascades (LCK, ZAP70, calcineurin, NFAT) to fine-tune cellular differentiation and anergy.
In HAP1 cells, disruption of EGR2 abolishes its dual roles in driving myelination gene expression and enforcing T-cell anergy checkpoints. The near-haploid background ensures that a single-allele knockout suffices to eliminate functional protein, reducing genetic buffering and background noise. This model permits direct assessment of EGR2 loss on target gene transcription, protein interactions, and signaling pathway responsiveness, making it ideal for dissecting the molecular mechanisms underlying peripheral neuropathies and immune disorders.
Researchers can employ this EGR2 knockout model to investigate Charcot-Marie-Tooth disease type 1D and congenital hypomyelinating neuropathy by measuring MPZ and PMP22 expression via RT-qPCR or western blotting. In immunology, the cells can be used to explore T-cell anergy through analysis of FASL induction, NFAT translocation, and apoptosis assays. Transcriptome-wide alterations can be mapped by RNA-seq, while EGR2 binding site occupancy can be examined by ChIP-qPCR. The polyclonal population is also suitable for functional genomic screens and drug discovery efforts targeting EGR2-dependent pathways. For further details or custom requests, please contact Ascent Research.
