［1］Maruyama H, Morino H,Ito H, et al. Mutations of optineurin in amyotrophic lateral sclerosis［J］. Nature,2010,465(7295):223-226.
［2］Van Blitterswijk M, van Vught PW, van Es MA, et al. Novel optineurin mutations in sporadic amyotrophic lateral sclerosis patients［J］. Neurobiol Aging, 2012, 33(5):1016.
［3］Li Y, Kang J, Horwitz M S. Interaction of an adenovirus E3 14.7-kilodalton protein with a novel tumor necrosis factor alpha-inducible cellular protein containing leucine zipper domains［J］.Mol Cell Biol,1998,18(3):1601-1610.
［4］Ying H, Yue BY. Cellular and molecular biology of optineurin［J］.Int Rev Cell Mol Biol,2012,294:223-258.
［5］Obazawa M, Mashima Y, Sanuki N, et al. Analysis of porcine optineurin and myocilin expression in trabecular meshwork cells and astrocytes from optic nerve head［J］. Invest Ophthalmol Vis Sci,2004,45(8):2652-2659.
［6］Maruyama H, Kawakami H. Optineurin and amyotrophic lateral sclerosis［J］. Geriatr Geronto Int,2013,13(3):528-532.
［7］Sahlender DA, Roberts RC, Arden SD, et al. Optineurin links myosin VI to the Golgi complex and is involved in Golgi organization and exocytosis［J］.J Cell Biol, 2005,169(2):285-295.
［8］Osawa T, Mizuno Y, Fujita Y, et al. Optineurin in neurodegenerative diseases［J］. Neuropathology,2011,31(6):569-574.
［9］del Toro D, Alberch J, Lázaro-Diéguez F, et al. Mutant huntingtin impairs post-Golgi trafficking to lysosomes by delocalizing optineurin/Rab8 complex from the Golgi apparatus［J］. Mol Biol Cell,2009,20(5):1478-1492.
［10］Ito H, Nakamura M, Komure O, et al. Clinicopathologic study on an ALS family with a heterozygous E478G optineurin mutation［J］. Acta Neuropathol, 2011, 122(2): 223-229.
［11］Gonatas NK, Stieber A, Gonatas JO. Fragmentation of the Golgi apparatus in neurodegenerative diseases and cell death［J］.J Neurol Sci,2006,246(1):21-30.
［12］Blokhuis A M, Groen E J N, Koppers M, et al. Protein aggregation in amyotrophic lateral sclerosis［J］. Acta Neuropathol,2013,125(6):777-794.
［13］Korac J, Schaeffer V, Kovacevic I, et al. Ubiquitin-independent function of optineurin in autophagic clearance of protein aggregates［J］. J Cell Sci,2013, 126(2):580-592.
［14］Todde V, Veenhuis M, Van Der Klei IJ. Autophagy: principles and significance in health and disease［J］. Biochim Biophys Acta,2009,1792(1):3-13.
［15］Wagner S, Carpentier I, Rogov V, et al. Ubiquitin binding mediates the NF-κB inhibitory potential of ABIN proteins［J］. Oncogene, 2008, 27(26): 3739-3745.
［16］Wild P, Farhan H, McEwan DG,et al. Phosphorylation of the autophagy receptor optineurin restricts Salmonella growth［J］. Science, 2011, 333(6039):228-233.
［17］Wong YC, Holzbaur ELF. Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation［J］. Proc Natl Acad Sci USA, 2014, 111(42): E4439-4448. 
［18］Swarup G, Nagabhushana A.Optineurin, a multifunctional protein involved in glaucoma, amyotrophic lateral sclerosis and antiviral signalling［J］. J Biosci, 2010,35(4):501-505.
［19］Cirulli ET, Lasseigne BN, Petrovski S, et al. Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways［J］. Science,2015,347(6229): 1436-1441.
［20］Freischmidt A, Wieland T, Richter B, et al. Haploinsufficiency of TBK1 causes familial ALS and fronto-temporal dementia［J］. Nat Neurosci,2015,18(5): 631-636.
［21］Shen WC, Li HY, Chen GC, et al. Mutations in the ubiquitin-binding domain of OPTN/optineurin interfere with autophagy-mediated degradation of misfolded proteins by a dominant-negative mechanism［J］. Autophagy,2015,11(4):685-700.
［22］Zhang X,Li L,Chen S,et al. Rapamycin treatment augments motor neuron degeneration in SOD1G93A mouse model of amyotrophic lateral sclerosis［J］. Autophagy,2011,7(4): 412-425.
［23］Wang IF, Guo BS, Liu YC, et al. Autophagy activators rescue and alleviate pathogenesis of a mouse model with proteinopathies of the TAR DNA-binding protein 43［J］.Proc Natl Acad Sci,2012,109(37):15024-15029.
［24］Zhu G, Wu CJ, Zhao Y, et al. Optineurin negatively regulates TNFα-induced NF-κB activation by competing with NEMO for ubiquitinated RIP［J］. Curr Biol, 2007,17(16):1438-1443.
［25］Su XW, Broach JR, Connor JR,et al. Genetic heterogeneity of amyotrophic lateral sclerosis: implications for clinical practice and research［J］.Muscle Nerve, 2014,49(6):786-803.
［26］Akizuki M, Yamashita H, Uemura K, et al. Optineurin suppression causes neuronal cell death via NF-kappaB pathway［J］.J Neurochem,2013,126(6):699-704.
［27］Camandola S, Mattson MP. NF-κB as a therapeutic target in neurodegenerative diseases［J］.Expert Opin Ther Targets, 2007, 11(2): 123-132.
［28］Ying H, Yue BY. Cellular and molecular biology of optineurin［J］. Int Rev Cell Mol Biol, 2012, 294: 223-258.
［29］Turturro S, Shen X, Shyam R, et al. Effects of mutations and deletions in the human optineurin gene［J］.Springerplus,2014,3(1):1-16. 
［30］Deng HX, Bigio EH, Zhai H, et al. Differential involvement of optineurin in amyotrophic lateral sclerosis with or without SOD1 mutations［J］.Arch Neurol, 2011,68(8):1057-1061. 
［31］Kamada M, Izumi Y, Ayaki T, et al. Clinicopathologic features of autosomal recessive amyotrophic lateral sclerosis associated with optineurin mutation［J］. Neuropathology,2014,34(1): 64-70.
［32］Gurney M E, Pu H, Chiu A Y, et al. Motor neuron degeneration in mice that express a human Cu, Zn superoxide dismutase mutation［J］.Science,1994,264(5166): 1772-1775.
［33］Wegorzewska I, Bell S, Cairns NJ, et al. TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration［J］.Proc Natl Acad Sci USA, 2009,106(44): 18809-18814.