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dc.contributor.authorYing, H
dc.contributor.authorYue, BY
dc.date.accessioned2016-05-10T15:48:20Z
dc.date.available2016-05-10T15:48:20Z
dc.date.issued2016-03
dc.identifier.bibliographicCitationYing, H. and Yue, B. Y. J. T. Optineurin: The autophagy connection. Exp Eye Res. 2016. 144: 73-80. DOI: 10.1016/j.exer.2015.06.029.en_US
dc.identifier.issn0014-4835
dc.identifier.urihttp://hdl.handle.net/10027/20559
dc.descriptionThis is the author’s version of a work that was accepted for publication in Experimental Eye Research. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Experimental Eye Research, 2016. 144: 73-80. DOI: 10.1016/j.exer.2015.06.029.en_US
dc.description.abstractOptineurin is a cytosolic protein encoded by the OPTN gene. Mutations of OPTN are associated with normal tension glaucoma and amyotrophic lateral sclerosis. Autophagy is an intracellular degradation system that delivers cytoplasmic components to the lysosomes. It plays a wide variety of physiological and pathophysiological roles. The optineurin protein is a selective autophagy receptor (or adaptor), containing an ubiquitin binding domain with the ability to bind polyubiquitinated cargoes and bring them to autophagosomes via its microtubule-associated protein 1 light chain 3-interacting domain. It is involved in xenophagy, mitophagy, aggrephagy, and tumor suppression. Optineurin can also mediate the removal of protein aggregates through an ubiquitin-independent mechanism. This protein in addition can induce autophagy upon overexpression or mutation. When overexpressed or mutated, the optineurin protein also serves as a substrate for autophagic degradation. In the present review, the multiple connections of optineurin to autophagy are highlighted.en_US
dc.description.sponsorshipThis work has been supported by grants (EY018828 and EY001792) from the National Eye Institute, Bethesda, MD, an unrestricted departmental grant from Research to Prevent Blindness, New York, NY; and a grant award G2013110 from BrightFocus Foundation, Clarksburg, MD.en_US
dc.publisherElsevier Inc.en_US
dc.subjectAggrephagyen_US
dc.subjectAmyotrophic lateral sclerosis (ALS)en_US
dc.subjectAutophagyen_US
dc.subjectAutophagy induceren_US
dc.subjectAutophagy receptoren_US
dc.subjectMitophagyen_US
dc.subjectNormal tension glaucoma (NTG)en_US
dc.subjectOptineurin (OPTN)en_US
dc.subjectProtein aggregateen_US
dc.subjectTumor suppressoren_US
dc.subjectUbiquitin–proteasome system (UPS)en_US
dc.subjectXenophagyen_US
dc.titleOptineurin: The autophagy connection.en_US
dc.typeArticleen_US


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