The ING4 Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the ING4 gene has been disrupted in the human haploid HAP1 cell line, providing a constitutive loss-of-function model for investigating ING4-mediated tumor suppression and chromatin regulation.
HAP1 cells are a near-haploid, adherent cell line with fibroblast-like morphology, originally derived from the KBM-7 chronic myeloid leukemia cell line. Their haploid nature simplifies genetic knockout studies by allowing clean functional readouts without compensation from a second allele, making this background ideal for functional genomics, signal transduction research, and drug screening applications.
ING4 is a type II tumor suppressor that associates with histone acetyltransferase complexes containing HBO1/MYST2, MOZ/MYST3, and MORF/MYST4 to modulate histone H3 and H4 acetylation. It enhances p53-dependent transcription of pro-apoptotic and cell cycle arrest genes such as p21 and Bax, while repressing NF-??B activity through direct interaction with p65, thereby downregulating targets like COX-2 and MMPs. ING4 also inhibits HIF-1??-mediated expression of VEGF and GLUT1, attenuating angiogenesis. Upstream regulators include p53, DNA damage, HIF-1??, and miR-650, positioning ING4 at a key intersection of stress and growth signaling.
Disruption of ING4 in the haploid HAP1 background relieves constraints on NF-??B and HIF-1?? pathways and diminishes p53-dependent transcriptional activation, offering a high-confidence system for phenotypic screening and mechanistic dissection of cross-talk among these pathways. The absence of a wild-type allele eliminates compensatory effects, enabling precise interrogation of ING4 functions.
This polyclonal knockout population is suitable for western blotting, RT-qPCR, and RNA-seq to assess expression of downstream targets; ChIP-qPCR for histone acetylation profiling; and functional assays including apoptosis, cell cycle, migration, invasion, and reporter assays for p53, NF-??B, or HIF-1?? activity. Drug sensitivity testing further supports oncology drug discovery. For additional details, please contact Ascent Research.
