Human BDKRB2 Stable Cell Line - HUVECs

The BDKRB2 gene encodes the bradykinin B2 receptor, a G protein-coupled receptor (GPCR) that is a major mediator of the physiological and pathological effects of bradykinin (a 9-amino acid peptide released during inflammation and tissue damage). The B2 receptor is constitutively expressed in a variety of tissues, including vascular endothelium, smooth muscle, and sensory neurons. Upon activation, BDKRB2 triggers the phosphatidylinositol-calcium second messenger system, leading to strong vasodilation, increased vascular permeability, and activation of pain fibers. In addition to its role in acute inflammation, the BDKRB2 signaling pathway is involved in angiogenesis, wound healing, and blood pressure regulation, and frequently interacts with the renin-angiotensin system. In oncology, BDKRB2 has been identified as an oncogene for various malignancies, including triple-negative breast cancer, hepatocellular carcinoma, and glioma. Activation of BDKRB2 promotes tumor cell migration, invasion, and epithelial-mesenchymal transition (EMT) by activating the ERK1/2 and PI3K/Akt signaling pathways. High expression of BDKRB2 is typically associated with more aggressive tumor phenotypes and lower patient survival.

A stable BDKRB2 cell line constructed in the context of human umbilical vein endothelial cells (HUVECs) is the gold standard model for studying vascular biology, inflammation, and cancer-related angiogenesis. HUVECs provide a physiologically relevant environment for studying endothelial function and vascular leakage mechanisms. Stable overexpression of BDKRB2 in these cells allows for detailed mapping of bradykinin-induced signaling pathways and their impact on endothelial barrier integrity. This product has wide applications in the pharmaceutical industry for high-throughput screening of B2 receptor antagonists, which are candidate drugs for the treatment of hereditary angioedema, diabetic retinopathy, and chronic inflammatory pain. Furthermore, the BDKRB2-HUVEC cell line is a valuable tool for studying how the kallikrein-kinin system promotes the pre-metastatic microenvironment and tumor-associated vascular remodeling. This model provides crucial data for developing drugs that selectively block BDKRB2-mediated vascular leakage and tumor progression without interfering with other important cardiovascular functions, offering a comprehensive platform for drug discovery and mechanistic studies.