This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population in which the human IL17RB gene has been disrupted. As a polyclonal pool, the cells carry heterogeneous editing events, providing a robust loss-of-function model without single-cell cloning. This population enables investigation of IL17RB-dependent signaling in a defined host background and is suitable for expansion while maintaining the knockout phenotype.
UM-UC-3 is an epithelial cell line derived from a human bladder transitional cell carcinoma, characterized by a TP53 mutation commonly found in high-grade bladder cancers. Its tumorigenic properties and widely used status in cancer research make it a relevant model for studying invasive bladder carcinoma. The epithelial morphology and genetic background support analyses of signal transduction, migration, and inflammation-associated oncogenic processes.
IL17RB encodes a receptor that binds the cytokines IL17B and IL25 (IL-17E). Upon ligand engagement, the receptor recruits the adaptor Act1 (TRAF3IP2) and TRAF6 to activate the NF-??B and MAPK cascades, including ERK, p38, and JNK. This signaling drives transcriptional induction of pro-inflammatory targets such as CCL20, CXCL1, IL-6, and TNF??, and promotes secretion of chemokines and cytokines that orchestrate type 2 immune responses and tissue inflammation.
In bladder cancer, IL17RB-mediated signaling contributes to an inflammatory microenvironment that may support tumor progression, angiogenesis, and immune modulation. Knocking out IL17RB in the TP53-mutant UM-UC-3 background allows researchers to dissect the specific contributions of IL17B/IL25 pathways to proliferation, migration, and cytokine output, and to explore crosstalk between IL17 signaling and TP53 dysfunction in malignancy.
Typical applications include stimulation with recombinant IL17B or IL25 followed by assessment of NF-??B and MAPK activation via phospho-specific western blotting or kinase assays. Downstream effects can be quantified by RT-qPCR or ELISA for cytokines like IL-6 and CXCL1. Functional assays such as migration/invasion and proliferation studies further define the role of IL17RB in bladder cancer aggressiveness. This knockout model also serves as a platform for drug discovery targeting the IL17 axis. For further details or to request a technical consultation, please contact Ascent Research.
