The EIF4A2 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human EIF4A2 gene. This product provides a heterogeneous pool of HAP1 cells harboring gene disruptions introduced by CRISPR/Cas9-mediated genome editing, generating a loss-of-function model suitable for dissecting EIF4A2-dependent cellular processes. The polyclonal format preserves genetic diversity while eliminating functional EIF4A2 protein expression, enabling robust functional studies without the need for single-cell cloning.
The HAP1 cell line is a near-haploid human leukemic cell line derived from the KBM-7 chronic myeloid leukemia model. Possessing a haploid karyotype that facilitates straightforward gene targeting and phenotypic analysis, HAP1 cells are widely employed as a genetic perturbation platform for investigating oncogenic signaling, apoptosis, and drug sensitivity. The leukemic origin offers a disease-relevant context for studying translation control mechanisms frequently dysregulated in hematological malignancies.
EIF4A2 encodes an ATP-dependent DEAD-box RNA helicase functioning as the enzymatic core of the eIF4F translation initiation complex. Within this complex, EIF4A2 binds eIF4G and eIF4E, and together with cofactors eIF4B and eIF4H, unwinds 5′ UTR secondary structures to promote ribosome recruitment and cap-dependent translation. Its activity is modulated by the mTORC1/4E-BP1 axis, as well as by PI3K/Akt and MAPK/ERK cascades downstream of growth factor receptors. This regulatory network enables selective translation of mRNAs with structured 5′ UTRs, including key oncogenic transcripts such as MYC, CCND1, BCL2, and VEGF, linking EIF4A2 to cell proliferation, survival, and angiogenesis.
In the HAP1 leukemic background, EIF4A2 knockout creates a physiologically pertinent model for studying translation-dependent oncogenic networks. Given the prevalence of mTOR pathway hyperactivation in myeloid leukemias, these cells allow researchers to assess the consequences of EIF4A2 loss on downstream targets and pathways. The near-haploid genome minimizes genetic redundancy, enhancing the penetrance of the knockout phenotype and simplifying data interpretation in assays measuring growth, viability, and apoptotic responses.
These polyclonal knockout cells are suited for applications such as monitoring cap-dependent translation via polysome profiling, quantifying target mRNA translation with luciferase reporters, and examining EIF4A2’s role in leukemic cell survival through flow cytometry-based apoptosis assays. They also enable RNA immunoprecipitation studies to map EIF4A2?CmRNA interactions and drug target validation using eIF4F inhibitors like rocaglates. Additional uses include functional genomics screens and complementation studies. For technical inquiries and ordering information, please contact Ascent Research.
