The IRF2BPL Knockout NCI-H1975 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the IRF2BPL gene in the human NCI-H1975 lung adenocarcinoma cell line. This polyclonal knockout format provides a heterogeneous pool of genetically modified cells, enabling robust loss-of-function analyses while avoiding clonal selection biases. The CRISPR/Cas9-mediated gene disruption renders the cells a versatile model for studying IRF2BPL function in a disease-relevant cellular context.
NCI-H1975 cells originate from a non-smoking female patient with lung adenocarcinoma and carry EGFR L858R/T790M mutations, which are associated with sensitivity and acquired resistance to EGFR tyrosine kinase inhibitors. This cell line is a well-established model for investigating EGFR-driven oncogenesis and therapeutic resistance mechanisms. The introduction of an IRF2BPL knockout into this genetic background creates a powerful tool for dissecting the interplay between IRF2BPL-mediated regulation and mutant EGFR signaling.
IRF2BPL encodes a nuclear protein containing a C-terminal RING finger domain, acting as a putative E3 ubiquitin ligase and transcriptional repressor. The protein physically interacts with transcription factors IRF2 and CUX1, as well as ubiquitin-conjugating enzymes, thereby linking transcriptional regulation to the ubiquitin-proteasome system. Its transcriptional repression activity and potential E3 ligase function implicate it in modulating downstream effectors such as neuronal genes SYN1 and GRIN2B, and its expression may be influenced by candidate upstream regulators SOX2 and PAX6. Through these interactions, IRF2BPL interfaces with signaling pathways including Wnt/??-catenin, Notch, and interferon signaling.
In the NCI-H1975 lung adenocarcinoma background, IRF2BPL knockout allows investigation of the gene??s contributions to cancer cell proliferation, migration, and drug sensitivity. This model is particularly suited to exploring whether IRF2BPL exerts tumor-suppressive or oncogenic activities and how its loss impacts EGFR signaling dynamics. The convergence of neurodevelopmental regulatory programs with lung adenocarcinoma pathophysiology offers a unique experimental system for uncovering novel mechanisms.
Typical research applications for this knockout cell pool include confirmation of IRF2BPL disruption via western blotting and RT-qPCR, phenotypic assessment through cell proliferation and migration assays, and drug sensitivity profiling against EGFR inhibitors. Advanced studies can employ RNA-seq to map transcriptomic changes, co-immunoprecipitation to probe protein complexes, and ubiquitination assays to characterize E3 ligase activity. For further technical information or to place an order, please contact Ascent Research.
