The IGF2BP3 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, providing a loss-of-function model for studying the human IGF2BP3 gene. Generated from HEK293T host cells via target-gene disruption, this heterogeneous pool of edited cells enables investigation of IGF2BP3-dependent processes without clonal selection artifacts, making it suitable for a broad range of functional genomics and cancer biology applications.
HEK293T cells are derived from human embryonic kidney 293 cells and stably express the SV40 large T antigen. This enables high-copy episomal replication of plasmids carrying the SV40 origin of replication, resulting in exceptional transfection efficiency and recombinant protein expression. As an epithelial cell line, HEK293T is a standard model for viral packaging, inducible expression systems, and genetic perturbation studies. The knockout of IGF2BP3 in this background offers a technically convenient system to interrogate the gene??s regulatory roles in a well-characterized cellular context.
IGF2BP3 encodes an RNA-binding protein that stabilizes and enhances translation of target mRNAs by binding their 3′ UTRs. Key downstream targets include CD44, MYC, HMGA2, IGF2, and CTNNB1, which mediate its oncogenic effects on proliferation, migration, invasion, and apoptosis inhibition. Expression of IGF2BP3 is transcriptionally activated by the ??-catenin/TCF complex downstream of WNT signaling, and by MYC, TGF-??/SMAD, LIN28B, and SRC kinases. The protein interacts with IGF2BP1/2, RNA helicases (DDX6, DHX9), translation initiation factors (eIF4E, eIF4G), and hnRNP proteins to form mRNP complexes that control cytoplasmic mRNA fate.
The HEK293T polyclonal IGF2BP3 knockout model is particularly informative for dissecting post-transcriptional gene regulation in an epithelial background. The loss of IGF2BP3 allows researchers to assess its contribution to mRNA stability, localization, and translation without interference from endogenous protein. This system supports reconstitution experiments with mutant IGF2BP3 constructs, dose-titration studies, and combinatorial perturbations with other RNA-binding proteins or signaling regulators, providing a versatile platform for mechanistic and translational research.
Researchers can employ this knockout model for RNA immunoprecipitation to identify IGF2BP3-bound transcripts, polysome profiling to measure translational efficiency, and actinomycin D chase assays to evaluate mRNA stability. Phenotypic assays such as Transwell migration/invasion, MTT/BrdU proliferation, and Annexin V apoptosis staining are directly applicable. Additionally, these cells serve as a negative control for RNA-seq and pooled CRISPR screens. For additional technical information and support, please contact Ascent Research.
