Ninjurin-1 is a protein encoded by the NINJ1gene in humans.[5][6] This transmembrane protein plays a critical role in plasma membrane rupture during lytic cell death.[7] NINJ1 is involved in the terminal stages of cell rupture across various cell death pathways, including pyroptosis, necroptosis, and ferroptosis.[8] By disrupting cell membranes, NINJ1 facilitates the release of intracellular proteins, such as lactate dehydrogenase and various Damage Associated Molecular Patterns (DAMPs) into the extracellular environment, triggering inflammation.[7] Upon activation, NINJ1 assembles into a chain-like oligomer that forms a ring structure—dubbed the "Ninja Cutter"—which, like a cookie cutter, cuts and releases membrane disks, enabling cell rupture.[9]
NINJ1 is located on the long arm of chromosome 9 (9q22.31).[6]
Clinical Significance
Since NINJ1 is involved in inflammatory cell death and release of DAMPs that are important for immune response to infection, loss or inhibition of NINJ1 may promote susceptibility to bacterial infections. This is supported by studies using Ninj1-/- knockout mice, which are more susceptible to infection with C. rodentium compared to wild type mice.[8]
NINJ1 circulating plasma levels are elevated in patients with sepsis and correlate with disease severity and mortality, making NINJ1 a potential prognostic biomarker for sepsis monitoring. [10]
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Cardoso CC, Martinez AN, Guimarães PE, etal. (2007). "Ninjurin 1 asp110ala single nucleotide polymorphism is associated with protection in leprosy nerve damage". J. Neuroimmunol. 190 (1–2): 131–8. doi:10.1016/j.jneuroim.2007.07.015. PMID17825431. S2CID20637695.
Toyama T, Sasaki Y, Horimoto M, etal. (2005). "Ninjurin1 increases p21 expression and induces cellular senescence in human hepatoma cells". J. Hepatol. 41 (4): 637–43. doi:10.1016/j.jhep.2004.06.027. PMID15464245.
Chadwick BP, Heath SK, Williamson J, etal. (1998). "The human homologue of the ninjurin gene maps to the candidate region of hereditary sensory neuropathy type I (HSNI)". Genomics. 47 (1): 58–63. doi:10.1006/geno.1997.5084. PMID9465296.
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