The EIF3H Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 cell line, designed for targeted disruption of the EIF3H gene. This product provides a pooled population of edited cells, offering a versatile loss-of-function model system for studying the biological roles of EIF3H in human cells. Employing CRISPR/Cas9-mediated gene disruption, this polyclonal knockout cell pool is suited for applications requiring a heterogeneous knockout background, enabling robust and reproducible phenotypic screening without the constraints of single-clone variability.
HAP1 is a near-haploid human cell line originally isolated from the male KBM-7 chronic myeloid leukemia (CML) cell line. Its near-haploid karyotype simplifies genetic manipulation, as a single targeting event can produce functional gene knockouts, making it a widely adopted platform for arrayed and pooled CRISPR screens. HAP1 cells retain many signaling characteristics of CML progenitors and are amenable to high-throughput experimental workflows, including cell-based assays, drug response profiling, and functional genomics studies.
EIF3H encodes a critical scaffold subunit of the eukaryotic translation initiation factor 3 (eIF3) complex, which orchestrates cap-dependent translation initiation by bridging the 40S ribosomal subunit to mRNA. EIF3H specifically integrates mitogenic and nutrient signals downstream of the mTORC1 and PI3K/AKT pathways to modulate the selective translation of mRNAs encoding pro-proliferative and anti-apoptotic factors. Key upstream regulators include mTORC1, PI3K/AKT signaling, and the MYC transcription factor, while downstream targets encompass CCND1 (cyclin D1), MYC, BCL2, and VEGFA. EIF3H interacts directly with other eIF3 complex subunits (e.g., eIF3A, eIF3C, eIF3D), the 40S ribosomal subunit, and signaling effectors such as mTOR and S6K1, thereby linking growth signals to the translational machinery.
In the context of the HAP1 chronic myeloid leukemia-derived model, disruption of EIF3H provides a powerful system to interrogate how aberrant translational control contributes to leukemogenesis and cancer progression. EIF3H has been implicated in diverse malignancies, including breast cancer, hepatocellular carcinoma, prostate cancer, melanoma, and chronic myeloid leukemia, often through dysregulation of mTORC1-driven protein synthesis. Knockout of EIF3H in HAP1 cells enables the dissection of its specific contribution to cell cycle progression, survival signaling, and sensitivity to targeted therapies, thereby offering insights into the molecular dependencies of CML and other cancers.
This polyclonal knockout cell model is well-suited for a range of experimental approaches in translational control research and oncology. Representative applications include CRISPR-based genetic screens, drug target validation studies, and functional dissection of mTORC1-driven translation. Typical assays that can be employed with these cells include Western blotting for EIF3H and downstream effectors, RT-qPCR for transcriptional responses, polysome profiling to assess translation efficiency, cell viability assays (MTT/CellTiter-Glo), flow cytometry for cell cycle distribution, apoptosis detection via Annexin V, and colony formation assays. For further details on product specifications and technical support, please contact Ascent Research.
