The EIF4H Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the EIF4H gene. This product provides a heterogeneous pool of HAP1 cells carrying targeted disruptions in EIF4H, enabling robust interrogation of its role in translation initiation without the biases of clonal selection. The polyclonal format ensures that a broad spectrum of edited alleles is represented, making it a versatile tool for pooled screening and population-based biochemical assays.
HAP1 is a near-haploid human cell line with fibroblast-like morphology, derived from the chronic myeloid leukemia patient-derived KBM-7 cell line. It is male and adherent, featuring a haploid karyotype that greatly simplifies CRISPR/Cas9-mediated gene knockout by eliminating the need for biallelic editing. This genetic simplicity, combined with retention of key signaling networks, makes HAP1 an ideal host for generating clean loss-of-function models in translational and cancer biology research.
EIF4H encodes an RNA helicase cofactor that stimulates the activity of eIF4A, a core component of the eIF4F complex. EIF4H facilitates unwinding of secondary structures within the 5?? untranslated regions (UTRs) of mRNAs, thereby promoting ribosome scanning and cap-dependent translation initiation. Its activity is controlled by upstream signals such as mTORC1, 4E?BPs, eIF4E, MNK1/2, insulin, growth factors, and PKC. Within the eIF4F complex, EIF4H directly interacts with eIF4A, eIF4G, eIF4B, and PABPC1, and its loss disproportionately impairs translation of mRNAs with highly structured 5?? UTRs, including key oncogenes like MYC, CCND1, VEGF, and BCL2. Thus, EIF4H serves as a critical link between growth factor signaling and the synthesis of oncogenic proteins.
The haploid nature of HAP1 cells ensures that CRISPR-mediated disruption of EIF4H yields a constitutive loss-of-function phenotype without confounding effects from a second allele. In this polyclonal knockout population, attenuation of EIF4H activity is expected to reduce cap-dependent translation of structured mRNAs, suppress oncogene expression, and compromise cell growth. This model provides a genetically defined system to dissect the eIF4F-dependent translatome and to study how translational control couples to proliferation and survival pathways.
These EIF4H knockout cells are well suited for diverse research applications, including CRISPR knockout screening, translational control studies, cancer biology, drug target validation, and viral host factor identification. They can be employed in assays such as polysome profiling, dual-luciferase reporter assays with structured 5?? UTRs, RNA immunoprecipitation, co?immunoprecipitation, western blotting for downstream targets, proliferation assays, and silvestrol sensitivity testing. Their haploid background also supports forward genetic screens and genome-wide approaches. Researchers seeking further details or technical support are encouraged to contact Ascent Research.
