Inflammatory diseases: is ubiquitinated NEMO at the hub?
| Data(s) |
2004
|
|---|---|
| Resumo |
Many patients with Crohn's disease carry mutations in NOD2, a molecule that can both activate and attenuate the pro-inflammatory effects of NF-kappa B. Recent studies implicate NOD2-induced ubiquitination of the NF-kappa B regulator NEMO as a potential means of manipulating the NF-kappa B signal. |
| Identificador |
http://serval.unil.ch/?id=serval:BIB_A845825978C2 isbn:0960-9822 (Print) pmid:15620634 doi:10.1016/j.cub.2004.11.040 isiid:000226069400008 |
| Idioma(s) |
en |
| Fonte |
Current Biology, vol. 14, no. 24, pp. R1040-R1042 |
| Palavras-Chave | #Acetylmuramyl-Alanyl-Isoglutamine/metabolism; Bacteria/metabolism; Carrier Proteins/metabolism; Crohn Disease/genetics; Crohn Disease/metabolism; Humans; I-kappa B Kinase; Intracellular Signaling Peptides and Proteins/genetics; Intracellular Signaling Peptides and Proteins/metabolism; Mutation/genetics; NF-kappa B/metabolism; Nod2 Signaling Adaptor Protein; Protein Structure, Tertiary; Signal Transduction/physiology; Ubiquitin/metabolism |
| Tipo |
info:eu-repo/semantics/article article |
