The EBF3 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt EBF3 (Early B-cell Factor 3) expression in human HAP1 cells. This polyclonal knockout pool provides a genetically heterogeneous loss-of-function model, enabling robust assessment of EBF3-dependent phenotypes while avoiding clonal artifacts. The targeted disruption of EBF3 abrogates its transcription factor activity, facilitating investigation of its roles in neurodevelopment and tumor suppression.
HAP1 is a near-haploid, adherent fibroblast-like cell line derived from the KBM-7 chronic myeloid leukemia (CML) line. Its near-haploid karyotype simplifies genetic manipulation and facilitates functional genomics studies, including CRISPR screens. HAP1 cells are widely utilized for knockout-based research due to their stable growth characteristics and suitability for high-content imaging and biochemical assays.
EBF3 is a transcription factor critical for neuronal differentiation and B-cell development, operating downstream of Notch signaling and acting in concert with EBF1 and PAX5. It transcriptionally regulates genes such as CDKN1A (p21) and BCL2, linking it to cell cycle control and apoptosis. EBF3 interacts with ZNF423 and SMAD proteins, and its downstream targets include neuronal markers TUBB3 and NEFL. Disruption of EBF3 thus impairs Notch-mediated transcriptional programs, affecting neuronal and lymphoid differentiation pathways.
In the HAP1 context, EBF3 knockout provides a scalable platform for studying neurodevelopmental defects and cancer biology. Since HAP1 cells exhibit some neural crest-like features, the absence of EBF3 can unmask vulnerabilities in cell cycle checkpoints and differentiation programs relevant to glioblastoma and EBF3-related neurodevelopmental disorder (HADDS). The polyclonal nature mitigates clonal effects, making it ideal for high-throughput functional assays.
Researchers can employ this model in functional genomics to map EBF3-dependent gene networks via RNA-seq, or in drug screening to identify compounds that modulate neuronal differentiation or tumor suppression. Typical assays include Western blotting to confirm EBF3 loss, immunocytochemistry for TUBB3 and NEFL to assess neuronal marker expression, as well as proliferation and apoptosis assays to evaluate growth alterations. This product is suitable for investigations into Notch-driven malignancies and neurodevelopmental disease mechanisms. For further information, contact Ascent Research.
