Recombinant Mouse Ninjurin-1 (Ninj1), partial

Homophilic transmembrane adhesion molecule involved in various processes such as inflammation, cell death, axonal growth, cell chemotaxis and angiogenesis. Promotes cell adhesion by mediating homophilic interactions via its extracellular N-terminal adhesion motif (N-NAM). Involved in the progression of the inflammatory stress by promoting cell-to-cell interactions between immune cells and endothelial cells. Involved in leukocyte migration during inflammation by promoting transendothelial migration of macrophages via homotypic binding. Promotes the migration of monocytes across the brain endothelium to central nervous system inflammatory lesions. Acts as a regulator of Toll-like receptor 4 (TLR4) signaling triggered by lipopolysaccharide (LPS) during systemic inflammation; directly binds LPS. Acts as a mediator of both programmed and necrotic cell death. Plays a key role in the induction of plasma membrane rupture during programmed and necrotic cell death: oligomerizes in response to death stimuli to mediate plasma membrane rupture (cytolysis), leading to release intracellular molecules named damage-associated molecular patterns (DAMPs) that propagate the inflammatory response. Plays a role in nerve regeneration by promoting maturation of Schwann cells. Acts as a regulator of angiogenesis. Promotes the formation of new vessels by mediating the interaction between capillary pericyte cells and endothelial cells. Also mediates vascular functions in penile tissue as well as vascular formation. Promotes osteoclasts development by enhancing the survival of prefusion osteoclasts. Also involved in striated muscle growth and differentiation. Also involved in cell senescence in a p53/TP53 manner, possibly by acting as an indirect regulator of p53/TP53 mRNA translation.; Secreted form generated by cleavage, which has chemotactic activity. Acts as an anti-inflammatory mediator by promoting monocyte recruitment, thereby ameliorating atherosclerosis.