The IGF2R Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human IGF2R gene. This pooled loss-of-function model enables investigation of the receptor??s multifaceted roles in growth factor clearance, lysosomal enzyme trafficking, and TGF-?? activation without the biases of single-cell clonal selection.
HEK293T is a human embryonic kidney epithelial cell line stably expressing SV40 large T antigen. Its ability to support high-efficiency transient transfection and episomal plasmid replication has made it a dominant platform for recombinant protein expression, lentiviral and retroviral packaging, and large-scale functional genomics. The line??s rapid growth and robust transfectability facilitate CRISPR-based gene disruption and downstream phenotypic assays.
IGF2R, the cation-independent mannose-6-phosphate/insulin-like growth factor 2 receptor, is a 300 kDa transmembrane protein central to multiple regulatory networks. It binds mannose-6-phosphate-modified lysosomal hydrolases and, through adaptors such as AP-1, AP-2, GGA, TIP47, and Rab9, delivers them to lysosomes. Concurrently, IGF2R internalizes IGF2, preventing its interaction with IGF1R and thereby attenuating AKT1/mTOR pro-proliferative signaling. Moreover, the receptor processes latent TGF-?? into its active form, which engages SMAD2/3 to transduce growth-inhibitory signals. These functions position IGF2R at the intersection of lysosomal biogenesis, mitogenic suppression, and tumor-suppressive TGF-?? cascades.
Disruption of IGF2R in HEK293T cells is expected to impair lysosomal enzyme sorting, elevate IGF1R/AKT/mTOR activity due to reduced IGF2 clearance, and diminish TGF-??/SMAD signaling. The polyclonal nature of this knockout population captures diverse CRISPR-induced edits, enabling population-averaged analysis of crosstalk among lysosomal, growth factor, and cytokine pathways in a tractable epithelial model that endogenously expresses key effectors.
Applications span cancer biology (hepatocellular carcinoma, breast cancer, Wilms tumor), IGF axis and TGF-?? pathway interrogation, lysosomal storage disorder modeling (e.g., mucolipidosis type II), and target validation. Representative assays include phospho-AKT (Ser473) ELISA, TGF-?? luciferase reporters, lysosomal enzyme activity measurements, colony formation, migration, and MTT proliferation. Standard western blotting and RT-qPCR are recommended to confirm IGF2R ablation and monitor downstream markers. For further technical details or ordering, contact Ascent Research.
