Claudin-18/CLDN18.2 Protein-VLP, Human (HEK293)

CLDN18-VLPs (Claudin 18 virus-like particles) play a crucial role in alveolar fluid homeostasis by regulating the composition of tight junctions in alveolar epithelial cells, impacting ion transport, and solute permeability, potentially through the modulation of actin cytoskeleton organization and beta-2-adrenergic signaling. Essential for lung alveolarization and the maintenance of the paracellular alveolar epithelial barrier, CLDN18-VLPs contribute to epithelial progenitor cell proliferation and organ size regulation by controlling the subcellular localization of YAP1 and restricting its target gene transcription. Additionally, CLDN18-VLPs act as a negative regulator of RANKL-induced osteoclast differentiation, possibly by influencing the subcellular distribution of TJP2/ZO-2 and participating in bone resorption in response to calcium deficiency. They mediate the osteoprotective effects of estrogen independently of RANKL signaling pathways. Furthermore, CLDN18-VLPs are implicated in maintaining the alveolar microenvironment homeostasis by regulating pH and subsequent T-cell activation, indirectly contributing to the limitation of C. neoformans infection.