Valino-Rivas et al. Trends Mol Med. 2019;25(4):341-360. NIK as a Druggable Mediator of Tissue Injury.

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NIK as a Druggable Mediator of Tissue Injury.

1. Department of Nephrology and Hypertension, Instituto de Investigacion Sanitaria (IIS) Fundacion Jimenez Diaz, School of Medicine, Universidad Autonoma de Madrid (UAM), Red de Investigacion Renal (REDINREN), and Fundacion Renal Inigo Alvarez de Toledo (FRIAT), Madrid, Spain.  2. Departamento de Quimica Organica y Quimica Inorganica, Universidad de Alcala and REDINREN, Madrid, Spain.  3. Centro de Biologia Molecular Severo Ochoa, Consejo Superior de Investigaciones Cientificas de la UAM, Madrid, Spain.  4. These authors contributed equally. Electronic address:.


NF-kappaB-inducing kinase (NIK, MAP3K14) is best known as the apical kinase that triggers non-canonical NF-kappaB activation and by its role in the immune system. Recent data indicate a role for NIK expressed by non-lymphoid cells in cancer, kidney disease, liver injury, glucose homeostasis, osteosarcopenia, vascular calcification, hematopoiesis, and endothelial function. The spectrum of NIK-associated disease now ranges from immunodeficiency (when NIK is defective) to autoimmunity, cancer, sterile inflammation, fibrosis, and metabolic disease when NIK is overactive. The development of novel small-molecule NIK inhibitors has paved the way to test NIK targeting to treat disease in vivo, and may eventually lead to NIK targeting in the clinic. In addition, NIK activators are being explored for specific conditions such as myeloid leukemia.