The Il7r Knockout ID8 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the ID8 mouse ovarian surface epithelial cell line, engineered to disrupt the Il7r gene encoding the interleukin-7 receptor alpha chain (IL-7R??). This polyclonal population abolishes IL-7 responsiveness, offering a loss-of-function model for examining IL-7R-mediated signaling without clonal selection. The cells are supplied as a heterogeneous pool, suitable for applications where population-level responses are informative.
The ID8 host cell line originates from C57BL/6 mouse ovarian surface epithelium, a tissue involved in ovulation and repair. ID8 serves as a syngeneic model for ovarian carcinoma, faithfully recapitulating tumor progression when implanted into immunocompetent C57BL/6 mice. This background integrates epithelial biology and tumor immunology, making it ideal for studying oncogenic signaling in an immune-competent context.
The Il7r gene encodes the IL-7R?? chain, which pairs with the common gamma chain (??c) to form the IL-7 receptor. Upon IL-7 binding, the receptor activates JAK1 and JAK3, leading to STAT5 phosphorylation, as well as PI3K-AKT and Ras-MAPK cascades via Shc and Grb2. These pathways upregulate survival factors (Bcl-2), cell cycle promoters (Cyclin D1, c-Myc), and the kinase Pim1, while SOCS1 provides negative feedback. Upstream regulation involves Notch, Foxo1, and inflammatory cytokines. In Il7r-disrupted cells, these signals are nullified, preventing STAT5, AKT, and MAPK activation.
In ovarian cancer, IL-7R signaling can promote tumor cell proliferation, survival, and immune evasion. The Il7r knockout ID8 polyclonal cells enable dissection of these mechanisms by eliminating IL-7R?? expression and downstream signaling. This model is pertinent to severe combined immunodeficiency, T-cell acute lymphoblastic leukemia, autoimmune diseases, and ovarian adenocarcinoma research. The syngeneic C57BL/6 system permits in vivo tumor studies without immunodeficient host artifacts.
Applications include western blotting for phospho-STAT5, RT-qPCR for Bcl-2 or c-Myc, flow cytometry for IL-7R??, proliferation and apoptosis assays, RNA-seq, and migration/invasion experiments. They are also suited for high-throughput inhibitor screens targeting JAK-STAT or PI3K-AKT pathways, and for in vivo tumorigenicity assays. For more information, contact Ascent Research.
