The KAT6B Knockout NCI-H1975 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human KAT6B histone acetyltransferase gene in the NCI-H1975 lung adenocarcinoma line. This heterogeneous pool enables functional interrogation of KAT6B loss-of-function without clonal selection bias, offering a robust model for studying KAT6B-dependent cellular phenotypes. Each lot is validated for target-gene disruption and supplied as a ready-to-use culture.
The NCI-H1975 host cell line originates from the pleural effusion of a non-smoking female with lung adenocarcinoma and carries both EGFR L858R and T790M mutations. These genetic alterations confer sensitivity to first- and third-generation EGFR tyrosine kinase inhibitors and render the line a widely used model for acquired drug resistance in non-small cell lung cancer (NSCLC). Adherent epithelial morphology and retention of EGFR-driven signaling hallmarks make NCI-H1975 clinically relevant for targeted therapy research.
KAT6B is a histone acetyltransferase that functions as a transcriptional coactivator for Notch signaling. It acetylates histones H3 and H4 at promoters of Notch target genes, facilitating chromatin remodeling and gene activation. KAT6B interacts with NICD, CSL (RBP-J), and MAML1, and forms complexes with BRPF1, ING5, and EAF6. Downstream targets include HES1, HES5, HOXA genes, MYC, and CCND1, linking Notch activation to proliferation and differentiation.
In EGFR-mutant NCI-H1975 lung adenocarcinoma cells, KAT6B may intersect with oncogenic signaling networks to modulate tumor-relevant phenotypes. Notch pathway activity has been implicated in NSCLC progression and resistance to EGFR inhibitors, and this polyclonal knockout population provides a means to dissect the specific contributions of KAT6B to proliferation, apoptosis, and migration. The model enables investigation of HAT-mediated epigenetic regulation in a clinically pertinent adenocarcinoma background.
Typical research applications include examining KAT6B function in EGFR-driven adenocarcinoma, elucidating its role in Notch-dependent transcriptional programs, and evaluating KAT6B as a therapeutic target. Compatible assays encompass western blotting, RT-qPCR, RNA-seq, and ChIP-qPCR for expression and chromatin analyses, as well as functional readouts such as MTT proliferation, Annexin V apoptosis, migration/invasion, and EGFR inhibitor sensitivity profiling. For further information, please contact Ascent Research.
