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Review article
https://doi.org/10.18054/pb.v121-122i1-2.10627

Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?

Nikolina Prtenjaca   ORCID icon orcid.org/0000-0001-7744-904X
Marin Dominovic
Josip Peradinovic
Rozalija Šajn
Andrea Markovinovic   ORCID icon orcid.org/0000-0003-1656-3150
Ivana Munitic   ORCID icon orcid.org/0000-0002-5171-9950 ; University of Rijeka

Fulltext: english, pdf (730 KB) pages 23-34 downloads: 61* cite
APA 6th Edition
Prtenjaca, N., Dominovic, M., Peradinovic, J., Šajn, R., Markovinovic, A. & Munitic, I. (2020). Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?. Periodicum biologorum, 121-122 (1-2), 23-34. https://doi.org/10.18054/pb.v121-122i1-2.10627
MLA 8th Edition
Prtenjaca, Nikolina, et al. "Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?." Periodicum biologorum, vol. 121-122, no. 1-2, 2020, pp. 23-34. https://doi.org/10.18054/pb.v121-122i1-2.10627. Accessed 18 Jun. 2021.
Chicago 17th Edition
Prtenjaca, Nikolina, Marin Dominovic, Josip Peradinovic, Rozalija Šajn, Andrea Markovinovic and Ivana Munitic. "Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?." Periodicum biologorum 121-122, no. 1-2 (2020): 23-34. https://doi.org/10.18054/pb.v121-122i1-2.10627
Harvard
Prtenjaca, N., et al. (2020). 'Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?', Periodicum biologorum, 121-122(1-2), pp. 23-34. https://doi.org/10.18054/pb.v121-122i1-2.10627
Vancouver
Prtenjaca N, Dominovic M, Peradinovic J, Šajn R, Markovinovic A, Munitic I. Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?. Periodicum biologorum [Internet]. 2020 [cited 2021 June 18];121-122(1-2):23-34. https://doi.org/10.18054/pb.v121-122i1-2.10627
IEEE
N. Prtenjaca, M. Dominovic, J. Peradinovic, R. Šajn, A. Markovinovic and I. Munitic, "Optineurin Dysfunction in Amyotrophic Lateral Sclerosis: Why So Puzzling?", Periodicum biologorum, vol.121-122, no. 1-2, pp. 23-34, 2020. [Online]. https://doi.org/10.18054/pb.v121-122i1-2.10627

Abstracts

Mutations in optineurin have been linked to amyotrophic lateral sclerosis (ALS) a decade ago, but its exact role in the neurodegenerative process is still unclear. As a lysine 63 (K63) and methionine (M1) poly-ubiquitin 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-kB) and interferon regulatory factor 3 (IRF3), as well as in membrane-associated trafficking events including autophagy, maintenance of the Golgi apparatus, and exocytosis. Other studies 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.

Hrčak ID: 254646

URI
https://hrcak.srce.hr/254646

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