IL17RB Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the human IL17RB gene in the near-haploid HAP1 cell line. This product provides a loss-of-function model for investigating interleukin-17 receptor B (IL-17RB) signaling without the confounding presence of wild-type receptor. The polyclonal nature of the knockout pool reflects a heterogeneous population of edited cells, generated through CRISPR/Cas9-mediated gene disruption, eliminating the need for single-cell cloning and enabling robust functional studies. As a genetic screen-ready tool, this knockout model is designed for researchers exploring the IL-17RB axis in inflammatory and allergic disease contexts, offering a versatile platform for downstream mechanistic and pharmacological investigations.
The host HAP1 cell line is derived from the KBM-7 chronic myeloid leukemia line and retains a near-haploid karyotype, a unique feature that simplifies genetic manipulation and enhances the reliability of phenotypic screening. Its hematopoietic origin renders it a pertinent model for studying immune signaling and cancer biology, particularly in leukemic contexts. The near-haploid state minimizes the complexity of gene-editing outcomes, allowing for clear interpretation of loss-of-function phenotypes. HAP1 cells are widely employed in functional genomics screens, pathway dissection, and drug target validation studies due to their tractable genome and consistent growth characteristics.
IL17RB encodes the cognate receptor for the cytokines IL-17B and IL-25, which play pivotal roles in orchestrating type 2 immune responses and pro-inflammatory signaling. Upon ligand engagement, IL-17RB heterodimerizes with IL-17RA and recruits the adaptor Act1 (TRAF3IP2). This event triggers the activation of TRAF6 and TAK1, leading to downstream stimulation of the IKK complex, which in turn phosphorylates and activates NF-??B. Concurrently, MAPK cascades??including JNK, p38, and ERK??are mobilized, culminating in the activation of transcription factors AP-1 and C/EBP. These transcriptional regulators drive the expression of a battery of effector molecules, including the pro-inflammatory cytokines IL-6, IL-8, and TNF, the chemokines CCL2 and CCL20, and the Th2-type cytokines IL-4, IL-5, and IL-13. The pathway is subject to modulation by upstream signals such as IL-4, IL-13, and TSLP, while the IKK complex and MAPKs serve as critical nodes integrating IL-17RB-derived signals.
In the HAP1 near-haploid background, disruption of IL17RB provides a clean and interpretable system to dissect receptor-specific contributions to cell signaling. The absence of a second allele simplifies the readout of functional assays, making it an ideal host for studying the IL-25?CIL-17RB?CAct1 axis in hematopoietic cells. This knockout model enables the direct interrogation of IL-17RB dependency in NF-??B and MAPK activation, cytokine production, and cell migration. By contrasting knockout and parental cells, researchers can attribute signaling events specifically to IL-17RB, thereby clarifying its role in inflammatory cascades that may be relevant to leukemic cell behavior or immune cell function.
This IL17RB knockout cell pool is suited for a wide range of experimental applications, including the investigation of IL-25-driven Th2 responses, screening for small-molecule inhibitors of the IL-17RB pathway, functional genomics of allergic inflammation, and validation of drug targets in asthma, inflammatory bowel disease, and autoimmune conditions. Representative assays include western blotting for phospho-NF-??B and phospho-p38, RT-qPCR quantification of IL-6 and IL-4 transcripts, ELISA-based measurement of secreted IL-8 and CCL20, NF-??B luciferase reporter assays, flow cytometric analysis of IL-17RB surface expression, co-immunoprecipitation of IL-17RB?CIL-17RA complexes, and chemotaxis assays. For additional product information and technical support, please contact Ascent Research.
