Cited 13 times in
Autophagy in granular corneal dystrophy type 2
DC Field | Value | Language |
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dc.contributor.author | 김응권 | - |
dc.contributor.author | 최승일 | - |
dc.date.accessioned | 2017-02-24T03:42:59Z | - |
dc.date.available | 2017-02-24T03:42:59Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0014-4835 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/146422 | - |
dc.description.abstract | Autophagy is a lysosomal degradative process that is essential for cellular homeostasis and metabolic stress adaptation. Defective autophagy is involved in the pathogenesis of many diseases including granular corneal dystrophy type 2 (GCD2). GCD2 is an autosomal dominant disorder caused by substitution of histidine for arginine at codon 124 (R124H) in the transforming growth factor β-induced gene (TGFBI) on chromosome 5q31. Transforming growth factor β-induced protein (TGFBIp) is degraded by autophagy, but mutant-TGFBIp accumulates in autophagosomes and/or lysosomes, despite significant activation of basal autophagy, in GCD2 corneal fibroblasts. Furthermore, inhibition of autophagy induces cell death of GCD2 corneal fibroblasts through active caspase-3. As there is currently no pharmacological treatment for GCD2, development of novel therapies is required. A potential strategy for preventing cytoplasmic accumulation of mutant-TGFBIp in GCD2 corneal fibroblasts is to enhance mutant-TGFBIp degradation. This could be achieved by activation of the autophagic pathway. Here, we will consider the role and the potential therapeutic benefits of autophagy in GCD2, with focus on TGFBIp degradation, in light of the recently established role of autophagy in protein degradation. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.format.extent | 14~21 | - |
dc.language | English | - |
dc.publisher | Academic Press | - |
dc.relation.isPartOf | EXPERIMENTAL EYE RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Autophagy/physiology* | - |
dc.subject.MESH | Corneal Dystrophies, Hereditary/etiology | - |
dc.subject.MESH | Corneal Dystrophies, Hereditary/metabolism* | - |
dc.subject.MESH | Extracellular Matrix Proteins/genetics | - |
dc.subject.MESH | Extracellular Matrix Proteins/metabolism | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Lysosomes | - |
dc.subject.MESH | Proteolysis | - |
dc.subject.MESH | Transforming Growth Factor beta/genetics | - |
dc.subject.MESH | Transforming Growth Factor beta/metabolism | - |
dc.subject.MESH | Substances | - |
dc.subject.MESH | Extracellular Matrix Proteins | - |
dc.subject.MESH | Transforming Growth Factor beta | - |
dc.subject.MESH | betaIG-H3 protein | - |
dc.title | Autophagy in granular corneal dystrophy type 2 | - |
dc.type | Article | - |
dc.publisher.location | England | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Ophthalmology | - |
dc.contributor.googleauthor | Seung-Il Choi | - |
dc.contributor.googleauthor | Eung Kweon Kim | - |
dc.identifier.doi | 10.1016/j.exer.2015.09.008 | - |
dc.contributor.localId | A00831 | - |
dc.contributor.localId | A04099 | - |
dc.relation.journalcode | J00868 | - |
dc.identifier.eissn | 1096-0007 | - |
dc.identifier.pmid | 26386150 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0014483515300294 | - |
dc.subject.keyword | Autophagy | - |
dc.subject.keyword | Corneal fibroblasts | - |
dc.subject.keyword | ECM endocytosis | - |
dc.subject.keyword | GCD2 | - |
dc.subject.keyword | TGFBIp | - |
dc.contributor.alternativeName | Kim, Eung Kweon | - |
dc.contributor.alternativeName | Choi, Seung Il | - |
dc.contributor.affiliatedAuthor | Kim, Eung Kweon | - |
dc.contributor.affiliatedAuthor | Choi, Seung Il | - |
dc.citation.volume | 144 | - |
dc.citation.startPage | 14 | - |
dc.citation.endPage | 21 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL EYE RESEARCH, Vol.144 : 14-21, 2016 | - |
dc.date.modified | 2017-02-24 | - |
dc.identifier.rimsid | 48410 | - |
dc.type.rims | ART | - |
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