Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling? (CROSBI ID 292700)
Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija
Podaci o odgovornosti
Prtenjaca, Nikolina ; Dominovic, Marin ; Peradinovic, Josip ; Šajn, Rozalija ; Markovinovic, Andrea ; Munitic, Ivana
engleski
Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?
Mutations in optineurin have been linked to amyotrophic lateral sclero- sis (ALS) a decade ago, but its exact role in the neurodegenerative process is still unclear. As a lysine 63 (K63)- and methionine (M1)-linked polyubiq- uitin-binding protein, optineurin has been reported to act as an adaptor in inflammatory signaling pathways mediated via nuclear factor kappa-light- chain-enhancer of activated B cells (NF-κB) and interferon regulatory fac- tor 3 (IRF3), as well as in membrane-associated trafficking events including autophagy, maintenance of the Golgi apparatus, and exocytosis. Other stud- ies have demonstrated its role in other processes such as regulation of mitosis, transcription, necroptosis and apoptosis. However, many of the reported effects in cell models have been proven difficult to reproduce in optineurin animal models, demonstrating the challenges of extrapolation between model systems. Knowing that multifunctional proteins present a “nightmare” for researchers, to help navigating through this field, we address the most common controversies, open questions, and artefacts related to optineurin and its role in pathogenesis of ALS and other neurodegenerative diseases.
optineurin ; ALS
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nije evidentirano
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Podaci o izdanju
121-122 (1-2)
2020.
23-34
objavljeno
0031-5362
1849-0964
10.18054/pb.v121-122i1-2.10627
Povezanost rada
Biotehnologija u biomedicini (prirodno područje, biomedicina i zdravstvo, biotehničko područje)