The IGF2BP1 Knockout HAP1 Polyclonal Cells product consists of a polyclonal population of HAP1 cells with targeted disruption of the IGF2BP1 gene using CRISPR/Cas9-mediated gene editing. This polyclonal knockout cell pool is designed as a loss-of-function model for studying the roles of the RNA-binding protein IGF2BP1 in post-transcriptional gene regulation, cancer biology, and signal transduction. The CRISPR/Cas9 approach generates a heterogeneous knockout cell population, which is suitable for pooled screening and bulk functional assays without the need for clonal isolation.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line. Its near-haploid karyotype simplifies gene perturbation studies and is widely employed in functional genomic screens, including CRISPR knockout and synthetic lethality analyses. The HAP1 cells retain leukemic characteristics, making them a relevant model for hematological malignancy research, yet they also support general investigations of conserved molecular pathways. This host cell background provides a robust platform for dissecting the leukemic and oncogenic functions of IGF2BP1.
IGF2BP1 is an oncofetal RNA-binding protein that controls the stability, translation, and subcellular localization of numerous transcripts. It is transcriptionally activated by MYC and ??-catenin/TCF, and post-transcriptionally repressed by let-7 miRNA. IGF2BP1 binds and stabilizes target mRNAs, including MYC, CTNNB1 (??-catenin), CD44, and ACTB, through recognition of specific RNA motifs. It interacts with co-factors such as YBX1, ELAVL1 (HuR), STAU1, and FMRP, forming ribonucleoprotein complexes that enhance mRNA half-life and translation efficiency. Mechanistically, IGF2BP1-driven stabilization of MYC and CTNNB1 mRNAs upregulates proliferation-associated genes, promoting PI3K/AKT, MAPK/ERK, and Wnt/??-catenin signaling. Additionally, IGF2BP1 mediates mRNA transport to cellular protrusions, facilitating cell migration and invasion, thereby driving aggressive cancer phenotypes.
In HAP1 chronic myeloid leukemia cells, disruption of IGF2BP1 is expected to attenuate oncogenic mRNA stabilization and downstream proliferative and migratory signaling. This polyclonal knockout model allows researchers to evaluate the impact of IGF2BP1 loss on leukemia cell fitness, signal transduction, and gene expression programs in a near-haploid genetic background. It is particularly useful for investigating the dependency of leukemic cells on post-transcriptional regulation by RNA-binding proteins, as well as for synthetic lethality screens where IGF2BP1 may be a critical node. The model also provides a system to study cross-talk between MYC-driven transcriptional networks and IGF2BP1-mediated post-transcriptional control in hematopoietic malignancies.
This product is applicable to a wide range of functional genomics and cancer research applications. Researchers can employ the IGF2BP1 knockout HAP1 polyclonal cells in western blotting and RT-qPCR to confirm target depletion, in RNA immunoprecipitation (RIP) and RNA-seq to identify altered mRNA interactomes and transcriptomes, and in proliferation and migration assays to assess phenotypic consequences. The polyclonal nature supports pooled CRISPR screens and drug target validation in high-throughput formats. This model is also valuable for studying the roles of RNA-binding proteins in mRNA metabolism and oncogenic transformation. For further information or to request a quote, please contact Ascent Research.
