The IGF2R Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by targeted disruption of the IGF2R gene in the Jurkat host cell line. This polyclonal pool provides a loss-of-function model capturing heterogeneous editing typical of CRISPR/Cas9-mediated gene disruption, enabling robust functional studies without single-clone selection.
Jurkat is a human T lymphoblast cell line derived from a 14-year-old male with acute lymphoblastic leukemia and serves as a widely used CD4+ T-cell model for T-cell activation, signaling, and apoptosis studies.
IGF2R (cation-independent mannose-6-phosphate receptor) is a multifunctional receptor that scavenges IGF2 via clathrin-mediated endocytosis for lysosomal degradation, thereby limiting IGF1R-driven growth signals. It also transports mannose-6-phosphate-tagged lysosomal enzymes from the Golgi to lysosomes, and binds latent TGF-beta complexes to facilitate TGF-beta activation. Interacting partners include IGF2, M6P-modified lysosomal hydrolases, latent TGF-beta, uPAR, retinoic acid, and G proteins. Representative pathway components encompass IGF2, M6P-proteins, IGF2R, clathrin, adaptor proteins, lysosomes, TGF-beta, and IGF1R, coordinating growth factor clearance, lysosomal enzyme trafficking, and tumor-suppressive signaling.
In Jurkat T-leukemia cells, IGF2R knockout enables examination of disrupted growth factor regulation, lysosomal enzyme targeting, and TGF-beta signaling. Loss of receptor function can elevate extracellular IGF2, enhancing IGF1R anti-apoptotic cascades, while impairing lysosomal delivery and reducing TGF-beta-mediated growth inhibition. This model illuminates tumor-suppressive mechanisms and the interplay between endocytic trafficking and leukemic signaling.
Applications include cancer biology, tumor suppressor studies, growth factor signaling, lysosomal storage disease research, T-cell signaling, and apoptosis analysis. Representative assays such as Western blotting, RT-qPCR, flow cytometry, ELISA, immunofluorescence, lysosomal enzyme activity measurements, apoptosis detection, and phospho-signaling analysis support detailed mechanistic investigations. For further technical information, please contact Ascent Research.
