The IGF2BP3 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the IGF2BP3 gene has been disrupted via targeted gene editing in the Jurkat T lymphoblastoid cell line. This polyclonal pool comprises a heterogeneous mixture of edited alleles, providing a robust loss-of-function model to interrogate the post-transcriptional regulatory roles of IGF2BP3 without clonal selection bias. The product is designed for researchers investigating RNA-binding protein-mediated control of mRNA stability and translation in a T-cell context.
The Jurkat host cell line is an immortalized human T lymphocyte line originally established from the peripheral blood of a 14-year-old male with acute T cell leukemia (T-ALL). These cells are extensively used as a model system for T cell receptor signaling, activation, and apoptosis, and they retain key features of T lymphoblasts. The Jurkat background makes this knockout particularly relevant for studying leukemogenic mechanisms and T-cell malignancies.
IGF2BP3 (insulin-like growth factor 2 mRNA-binding protein 3) is an RNA-binding protein that specifically recognizes N6-methyladenosine (m6A) modifications on target mRNAs. Through direct binding, IGF2BP3 stabilizes transcripts and enhances their translation, thereby promoting the expression of critical oncogenes such as MYC and CD44, as well as cell-cycle regulators like CCND1 and ACTB. Its activity is regulated by upstream factors including the WNT/??-catenin pathway, the transcription factor MYC, and the RNA-binding protein LIN28B. IGF2BP3 interacts with translation initiation components (EIF4E), cytoplasmic poly(A)-binding protein PABPC1, and RNA trafficking proteins such as STAU1 and YBX1. In the Jurkat model, IGF2BP3 knockout disrupts the post-transcriptional stabilization of these target mRNAs, leading to reduced oncoprotein expression and attenuated proliferative signaling.
In the context of Jurkat cells, loss of IGF2BP3 provides a unique experimental system to dissect the contribution of m6A-mediated mRNA regulation to T-cell leukemia biology. Given that IGF2BP3 is frequently overexpressed in hematologic malignancies, its knockout in this T-ALL-derived line impairs the stabilization of transcripts encoding key components of the WNT/??-catenin and MYC pathways, thereby diminishing cell survival and clonogenic potential. This model thus enables the study of how RNA-binding proteins interface with core leukemogenic signaling networks, including ??-catenin/TCF/LEF transcriptional output and MYC-driven proliferation.
Researchers can employ the IGF2BP3 Knockout Jurkat Polyclonal Cells in a variety of applications, such as functional dissection of RNA-binding protein networks in T-cell leukemia, identification of IGF2BP3-regulated transcripts via RNA sequencing, and high-throughput screening for small-molecule inhibitors of IGF2BP3?CRNA interactions. Representative downstream assays include Western blotting and RT-qPCR to validate target expression, flow cytometry with Annexin V/PI staining for apoptosis, MTT-based proliferation assays, transwell migration and invasion tests, RNA immunoprecipitation to map binding sites, and luciferase reporter assays to assess translational control. For additional technical details, please contact Ascent Research.
