The GPR108 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the GPR108 gene. These cells feature targeted disruption of GPR108 via CRISPR/Cas9-mediated gene editing, resulting in a heterogeneous pool of cells with loss-of-function mutations. This product is validated for applications in innate immunity and inflammation research, offering a versatile model to dissect GPR108 signaling pathways.
The HAP1 cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) lineage. With its haploid genome, HAP1 cells are particularly amenable to knockout studies, as a single targeting event can generate complete gene disruption, avoiding the complexity of diploid compensation. This characteristic makes HAP1 an invaluable host for CRISPR-mediated knockout screens and targeted gene editing, enabling unambiguous genotype-phenotype correlations. The cells maintain key signaling pathways, including those involved in immune responses, making them suitable for studying GPCR function.
GPR108 encodes a G protein-coupled receptor that functions in innate immune recognition of bacterial components. The receptor is activated by bacterial lipopeptides such as FSL-1 and TLR2/TLR6 ligands, leading to downstream signaling through MyD88 adaptor interactions. GPR108 engagement triggers a cascade involving IRAK4 and TRAF6, culminating in IKK complex activation and subsequent NF-??B nuclear translocation. This pathway drives the transcription of pro-inflammatory cytokines, including IL-6 and TNF-??, thereby orchestrating antimicrobial responses. Additionally, GPR108 may couple to heterotrimeric G proteins, further diversifying its signaling outputs.
In HAP1 cells, GPR108 knockout abrogates ligand-induced NF-??B and MAPK activation, providing a clean loss-of-function model. The haploid background ensures complete disruption without residual signaling from an intact allele, enhancing the clarity of phenotypic outcomes. This model enables precise dissection of GPR108??s role in bacterial sensing and the validation of its interaction partners, such as MyD88 and TRAF6. Comparative studies with wild-type HAP1 cells allow researchers to attribute altered inflammatory responses specifically to GPR108 deficiency, facilitating pathway mapping and target validation.
The GPR108 Knockout HAP1 Polyclonal Cells support a broad range of experimental applications in innate immunity and inflammation research. They are ideally suited for NF-??B luciferase reporter assays, cytokine ELISA, western blotting for phospho-p65 and phospho-ERK, flow cytometry, bacterial stimulation assays, and qPCR for cytokine gene expression. These applications support ligand identification, inflammatory disease modeling, and anti-inflammatory drug screening. For additional information, please contact Ascent Research.
