Mouse Egl Nine Homolog 1 (EGLN1) ELISA Kit-Sandwich

Egl nine homolog 1 serves as a cellular oxygen sensor and, under normoxic conditions, catalyzes the post-translational modification of hypoxia-inducible factor (HIF) alpha proteins by forming 4-hydroxyproline. It targets a specific proline within the oxygen-dependent degradation (ODD) domains. Research involving the selective knockout of Egln1 in alveolar endothelial cells has demonstrated that this alteration can trigger spontaneous pulmonary hypertension (PH) in mice. This condition is characterized by significant pulmonary vascular remodeling, including vascular occlusion and muscularization, as well as increased right ventricular pressure and hypertrophy. Egln1 deficiency specifically leads to the proliferation of pulmonary artery smooth muscle cells and the activation of profibrotic signaling pathways in vascular endothelial cells, such as through modulation of the CXCL1/FoxM1 signaling pathway.