The IGF2BP1 knockout Jurkat polyclonal cells are a CRISPR/Cas9-edited population derived from the human T-cell leukemia Jurkat line, featuring targeted gene disruption of IGF2BP1. This polyclonal knockout format circumvents clonal selection, providing a mixed population of edited cells that collectively lack functional IGF2BP1 protein. This model enables robust loss-of-function studies without the biases introduced by single-cell cloning, making it ideal for investigating post-transcriptional gene regulation in a malignant T-cell context.
Jurkat cells originate from an adolescent with acute T-cell leukemia and are widely used to study T-cell receptor signaling, apoptosis, and oncogenic transformation. Their rapid growth, stable karyotype, and well-characterized signaling pathways??including NF-??B, MAPK, and PI3K/AKT??render them a versatile platform for leukemia research and drug discovery. This genetic background provides a disease-relevant environment to analyze IGF2BP1’s role in mRNA metabolism and T-ALL pathogenesis.
IGF2BP1 is an RNA-binding protein that stabilizes oncogenic mRNAs and enhances their translation, interacting with ELAVL1, hnRNP proteins, and the 40S ribosomal subunit. Its transcription is directly regulated by the ??-catenin/TCF complex downstream of Wnt/Frizzled/DVL signaling and by MYC. Key targets include MYC, CTNNB1, PTEN, and CD44 mRNAs; stabilization of these transcripts promotes cell cycle progression and survival. IGF2BP1 thus integrates Wnt, MAPK/ERK, and PI3K/AKT inputs to control the post-transcriptional oncogenic program.
Knockout of IGF2BP1 in Jurkat T-ALL cells disrupts this regulatory hub, leading to reduced stability and translation of target mRNAs such as MYC and CTNNB1. The resulting decrease in oncogenic protein levels impairs proliferation and sensitizes cells to apoptotic stimuli, recapitulating a therapeutically relevant vulnerability. This model allows precise dissection of IGF2BP1-dependent RNA regulons and evaluation of functional consequences in a leukemic context, supporting target validation studies.
Typical applications include RNA stability assays by RT-qPCR or RNA-seq, protein-level confirmation via western blotting, and functional assays such as apoptosis and proliferation measured by flow cytometry. RNA immunoprecipitation can map altered protein-RNA interactions, while migration/invasion assays assess metastatic potential. The model is valuable for drug screening, synthetic lethality studies, and mechanistic investigations into mRNA regulation in T-ALL. For detailed technical information, please contact Ascent Research.
