NIK as a Druggable Mediator of Tissue Injury.
MAP3K14
NIK
TWEAK
acute kidney injury
apoptosis
autoimmunity
cell death
chronic kidney disease
cirrhosis
diabetes
epigenetic
esteatohepatitis
hepatitis
inflammation
mantle lymphoma
myeloid leukemia
osteoporosis
sarcopenia
verteporfin
Journal
Trends in molecular medicine
ISSN: 1471-499X
Titre abrégé: Trends Mol Med
Pays: England
ID NLM: 100966035
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
05
12
2018
revised:
07
02
2019
accepted:
13
02
2019
pubmed:
31
3
2019
medline:
13
2
2020
entrez:
31
3
2019
Statut:
ppublish
Résumé
NF-κB-inducing kinase (NIK, MAP3K14) is best known as the apical kinase that triggers non-canonical NF-κB 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.
Identifiants
pubmed: 30926358
pii: S1471-4914(19)30040-1
doi: 10.1016/j.molmed.2019.02.005
pii:
doi:
Substances chimiques
Biomarkers
0
Protein Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
341-360Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.