In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The CBX4 Knockout BEAS-2B Cell Line provides a CRISPR/Cas9-edited loss-of-function model of the CBX4 gene in SV40-immortalized human bronchial epithelial cells. CBX4 functions as a transcriptional repressor within PRC1 and as a SUMO E3 ligase, modifying substrates such as HIPK2, CtBP, and PML, and is regulated by upstream kinase HIPK2. This knockout enables investigation of epigenetic silencing, SUMOylation, and epithelial differentiation in airway biology. It supports assays including ChIP-qPCR for H2AK119ub, western blotting for SUMO targets, TEER measurement, and senescence analysis, making it suitable for cancer, respiratory disease, and drug discovery research.
ASGR2 Knockout HAP1 Polyclonal Cells
Cat. No. ARG21946
Trp53 Knockout C57BL/6 MSC Cell Line
Cat. No. ARG44195
GSDME Knockout A2780 Polyclonal Cells
Cat. No. ARG35255
Bdh1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG37889
MCOLN1 Knockout 786O Polyclonal Cells
Cat. No. ARG5605
MCCC2 Knockout Raji Polyclonal Cells
Cat. No. ARG1527
The CBX4 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited knockout cell line that disrupts the CBX4 gene in SV40-immortalized human bronchial epithelial cells. By employing CRISPR/Cas9-mediated gene disruption, this model delivers a stable loss-of-function system for investigating CBX4-dependent transcriptional repression via Polycomb repressive complex 1 (PRC1) and SUMO E3 ligase activity. It avoids the off-target effects and transient nature of RNA interference, providing a reliable platform for long-term functional assays.
The BEAS-2B line originates from normal human bronchial epithelium immortalized with SV40 large T antigen, retaining key airway features such as polarized barrier formation, mucociliary clearance, and innate immune responsiveness. Its non-tumorigenic status makes it a physiologically relevant model for epithelial cell biology and respiratory disease research, free from oncogenic transformation artifacts. Integration of the CBX4 knockout thus enables direct interrogation of epigenetic regulators in a primary-like bronchial cell context.
CBX4 functions as a transcriptional repressor through PRC1, interacting with RING1 and BMI1 to catalyze H2AK119ub and compact chromatin. Additionally, as a SUMO E3 ligase, it facilitates SUMOylation of substrates including HIPK2, CtBP, PML, and itself, in cooperation with the E2 enzyme Ubc9. Upstream kinase HIPK2 and stress signals modulate CBX4 activity. Critical downstream targets comprise the INK4a/ARF locus and other developmentally controlled genes, linking CBX4 to senescence and differentiation pathways.
Within airway epithelial cells, CBX4 likely governs barrier integrity, differentiation, and innate defense programs. The BEAS-2B knockout model enables assessment of how loss of CBX4-mediated gene silencing affects tight junction composition, mucociliary clearance components, and inflammatory gene expression. Such perturbations are particularly relevant to respiratory diseases like COPD and asthma, where epithelial dysfunction and aberrant epigenetic regulation are central. This model thus offers a powerful tool for uncovering epigenetic contributions to pulmonary pathology.
Researchers can employ this knockout line in ChIP-qPCR for H2AK119ub and CBX4 binding, western blotting for CBX4 and SUMOylated proteins, and RT-qPCR of PRC1 targets. Functional studies may include senescence assays, TEER for barrier function, migration/invasion, and immunofluorescence localization. Additionally, it supports SUMOylation analyses via immunoprecipitation and complementation experiments with CBX4 variants. For further information or to discuss custom applications, please contact Ascent Research.
