The HRH1 Knockout 143B Polyclonal Cells are a heterogeneous population of 143B human osteosarcoma cells that have undergone CRISPR/Cas9-mediated disruption of the HRH1 gene, which encodes the histamine H1 receptor. This polyclonal product provides a loss-of-function model suitable for pooled screening and bulk functional assays, without clonal isolation. The genetic perturbation ablates HRH1 expression, enabling researchers to dissect histamine-dependent signaling pathways in a context highly relevant to both inflammation and cancer biology.
The 143B cell line is a subclone of the TE85 human osteosarcoma isolate, selected for its highly tumorigenic and metastatic properties. Lacking thymidine kinase (TK-), 143B cells serve as a robust model for osteosarcoma progression, including studies on tumor growth, angiogenesis, and metastasis. Their aggressive in vivo behavior makes them particularly valuable for evaluating genes implicated in osteosarcoma pathobiology and for preclinical drug testing.
The HRH1 protein is a G protein-coupled receptor activated by histamine, coupling primarily to the G??q/11 family. Ligand binding stimulates phospholipase C?? to produce IP? and DAG, mobilizing calcium and activating protein kinase C. These events drive NF-??B and p38 MAPK pathways, inducing expression of IL-6, IL-8, COX-2, iNOS, ICAM-1, and VCAM-1. Receptor regulation involves ??-arrestins and GRKs, while transcriptional control is exerted by cytokines such as IL-4, IL-13, TNF-??, and IFN-??.
In the 143B osteosarcoma background, this knockout cell population enables examination of HRH1??s contribution to tumor cell migration, invasion, and metastatic dissemination??processes potentially influenced by histamine-driven inflammation. By disrupting HRH1, researchers can assess how histaminergic signaling intersects with oncogenic pathways in a bone tumor microenvironment, providing insights into the receptor??s role beyond classical allergic responses.
Researchers can employ this product for a wide array of assays, including calcium flux measurements to monitor acute receptor desensitization, NF-??B luciferase reporter assays to quantify downstream transcriptional activity, and transwell migration or Matrigel invasion assays to evaluate metastatic potential. The cells are also suitable for testing small-molecule antagonists or biased ligands targeting HRH1 and for examining histamine-induced phospho-signaling events. In vivo, they can be used in xenograft models to study the effects of HRH1 loss on tumor growth and metastasis. For ordering or technical inquiries, please contact Ascent Research.
