The HRH1 Knockout AGS Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human AGS gastric adenocarcinoma cell line, with targeted disruption of the HRH1 gene. This polyclonal format provides a heterogeneous pool of cells carrying diverse loss-of-function mutations at the HRH1 locus, enabling population-level analysis of HRH1-dependent signaling and phenotypes without the constraints of single-clone variability.
AGS cells are an epithelial gastric adenocarcinoma line widely used as an in vitro model for gastric cancer research. They retain key oncogenic signaling pathways and exhibit malignant characteristics suitable for studying GPCR-driven proliferation and inflammation. This host background is clinically relevant for investigating histamine receptor function in gastric epithelial biology and disease.
HRH1 encodes the histamine H1 receptor, a Gq/11-coupled GPCR that, upon histamine binding, activates GNAQ/GNA11 to stimulate PLCB2. This generates IP3 and DAG second messengers; IP3 mobilizes intracellular calcium via ITPR receptors, while DAG activates PRKCA. PRKCA in turn phosphorylates MAPK1 (ERK2) and promotes NFKB1 (NF-??B) transcriptional activity, leading to expression of pro-inflammatory and proliferative genes. Receptor signaling is terminated by GRK2/GRK5-mediated phosphorylation and ARRB1/ARRB2-dependent desensitization and internalization.
In gastric cancer, HRH1 signaling can drive tumor-promoting inflammation and cell growth through ERK and NF-??B pathways. Disrupting HRH1 in AGS cells permits precise dissection of these mechanisms and evaluation of H1 receptor antagonists. This model is pertinent to conditions such as gastric cancer, peptic ulcer disease, and allergic disorders, where histamine-mediated signaling plays a pathogenic role.
These polyclonal knockout cells are suited for Western blot confirmation of HRH1 loss, RT-qPCR analysis of downstream genes like IL-8, calcium flux assays, MTT proliferation assays, and NF-??B luciferase reporter assays. They enable functional studies of histamine-dependent pathways in gastric cancer, screening of H1 receptor antagonists, and investigation of GPCR-driven inflammation. The polyclonal nature minimizes clonal artifacts and provides robust population-level data. For additional information or to integrate this model into your research projects, please contact Ascent Research.
