NINJ1 Protein, Mouse (Cell-Free, His)

NINJ1 Protein serves as a pivotal effector in programmed cell death, mediating plasma membrane rupture in necroptosis and pyroptosis. Downstream of Gasdermin or MLKL activation, NINJ1 oligomerizes in response to death stimuli, introducing hydrophilic faces of two alpha helices into the hydrophobic membrane, leading to the release of damage-associated molecular patterns (DAMPs) and propagating the inflammatory response. Additionally, NINJ1 acts as a regulator of Toll-like receptor 4 (TLR4) signaling during systemic inflammation by directly binding lipopolysaccharide (LPS). It contributes to leukocyte migration, transendothelial migration of macrophages, and promotes monocyte migration to central nervous system inflammatory lesions. Functioning as a homophilic transmembrane adhesion molecule, NINJ1 is involved in axonal growth, cell chemotaxis, angiogenesis, and cell-to-cell interactions between immune cells and endothelial cells. It plays diverse roles in nerve regeneration, angiogenesis, vascular formation, osteoclast development, striated muscle growth, and differentiation. The secreted form exhibits chemotactic activity and acts as an anti-inflammatory mediator by promoting monocyte recruitment, thereby ameliorating atherosclerosis.