Nerve injury-induced protein 1 (NINJ1)

Nerve injury-induced protein 1 (NINJ1, also known as Ninjurin-1) is a cell-surface adhesion molecule initially identified in Schwann cells and neurons following nerve injury. It is a double-transmembrane protein that mediates homophilic cell-cell adhesion and is crucial in axon growth, nerve repair, and regeneration. Beyond the nervous system, NINJ1 regulates cell migration, especially of leukocytes, and modulates inflammatory responses by facilitating immune cell infiltration into tissues. It plays a direct role in plasma membrane rupture during lytic cell death, contributing to the release of damage-associated molecular patterns (DAMPs) in inflammation. NINJ1 expression is upregulated in various neuroinflammatory, vascular, and neoplastic diseases and has been experimentally targeted to ameliorate outcomes in nerve injury, stroke, and autoimmunity. Its multifaceted pathophysiological functions and disease associations make it of high interest as a potential therapeutic target, although there are currently no approved drugs targeting NINJ1 directly[1][2][3][4][5][6][7][8][9].

Other names

Ninjurin-1Ninj1

Antibody blockade/interference with NINJ1 affects cell adhesion and inflammatory cell recruitment[1][4] NINJ1 inhibition reduces leukocyte infiltration and systemic inflammation[4][6] Experimental agents modulate NINJ1 to alter nerve regeneration, inflammation, or lytic cell death pathways