{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1363670320440834048.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1016/s0092-8674(01)00407-x"}},{"identifier":{"@type":"URI","@value":"https://api.elsevier.com/content/article/PII:S009286740100407X?httpAccept=text/xml"}},{"identifier":{"@type":"URI","@value":"https://api.elsevier.com/content/article/PII:S009286740100407X?httpAccept=text/plain"}},{"identifier":{"@type":"PMID","@value":"11439185"}},{"identifier":{"@type":"NAID","@value":"30010681760"}}],"dc:title":[{"@value":"An Unfolded Putative Transmembrane Polypeptide, which Can Lead to Endoplasmic Reticulum Stress, Is a Substrate of Parkin"}],"description":[{"notation":[{"@value":"A putative G protein-coupled transmembrane polypeptide, named Pael receptor, was identified as an interacting protein with Parkin, a gene product responsible for autosomal recessive juvenile Parkinsonism (AR-JP). When overexpressed in cells, this receptor tends to become unfolded, insoluble, and ubiquitinated in vivo. The insoluble Pael receptor leads to unfolded protein-induced cell death. Parkin specifically ubiquitinates this receptor in the presence of ubiquitin-conjugating enzymes resident in the endoplasmic reticulum and promotes the degradation of insoluble Pael receptor, resulting in suppression of the cell death induced by Pael receptor overexpression. Moreover, the insoluble form of Pael receptor accumulates in the brains of AR-JP patients. Here, we show that the unfolded Pael receptor is a substrate of Parkin, the accumulation of which may cause selective neuronal death in AR-JP."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1383670320440834050","@type":"Researcher","foaf:name":[{"@value":"Yuzuru Imai"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320440834053","@type":"Researcher","foaf:name":[{"@value":"Mariko Soda"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320440834052","@type":"Researcher","foaf:name":[{"@value":"Haruhisa Inoue"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320440834048","@type":"Researcher","foaf:name":[{"@value":"Nobutaka Hattori"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320440834051","@type":"Researcher","foaf:name":[{"@value":"Yoshikuni Mizuno"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320440834049","@type":"Researcher","foaf:name":[{"@value":"Ryosuke Takahashi"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00928674"}],"prism:publicationName":[{"@value":"Cell"}],"dc:publisher":[{"@value":"Elsevier BV"}],"prism:publicationDate":"2001-06","prism:volume":"105","prism:number":"7","prism:startingPage":"891","prism:endingPage":"902"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["https://www.elsevier.com/tdm/userlicense/1.0/","https://www.elsevier.com/legal/tdmrep-license","http://www.elsevier.com/open-access/userlicense/1.0/"],"url":[{"@id":"https://api.elsevier.com/content/article/PII:S009286740100407X?httpAccept=text/xml"},{"@id":"https://api.elsevier.com/content/article/PII:S009286740100407X?httpAccept=text/plain"}],"createdAt":"2002-07-25","modifiedAt":"2025-09-25","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Protein%20Folding","dc:title":"Protein Folding"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Death","dc:title":"Cell Death"},{"@id":"https://cir.nii.ac.jp/all?q=Biochemistry,%20Genetics%20and%20Molecular%20Biology(all)","dc:title":"Biochemistry, Genetics and Molecular Biology(all)"},{"@id":"https://cir.nii.ac.jp/all?q=Recombinant%20Fusion%20Proteins","dc:title":"Recombinant Fusion Proteins"},{"@id":"https://cir.nii.ac.jp/all?q=Ubiquitin-Protein%20Ligases","dc:title":"Ubiquitin-Protein Ligases"},{"@id":"https://cir.nii.ac.jp/all?q=Brain","dc:title":"Brain"},{"@id":"https://cir.nii.ac.jp/all?q=Receptors,%20Cell%20Surface","dc:title":"Receptors, Cell Surface"},{"@id":"https://cir.nii.ac.jp/all?q=Cysteine%20Proteinase%20Inhibitors","dc:title":"Cysteine Proteinase Inhibitors"},{"@id":"https://cir.nii.ac.jp/all?q=Endoplasmic%20Reticulum","dc:title":"Endoplasmic Reticulum"},{"@id":"https://cir.nii.ac.jp/all?q=Precipitin%20Tests","dc:title":"Precipitin Tests"},{"@id":"https://cir.nii.ac.jp/all?q=Acetylcysteine","dc:title":"Acetylcysteine"},{"@id":"https://cir.nii.ac.jp/all?q=Ligases","dc:title":"Ligases"},{"@id":"https://cir.nii.ac.jp/all?q=Microscopy,%20Fluorescence","dc:title":"Microscopy, Fluorescence"},{"@id":"https://cir.nii.ac.jp/all?q=Parkinsonian%20Disorders","dc:title":"Parkinsonian Disorders"},{"@id":"https://cir.nii.ac.jp/all?q=Two-Hybrid%20System%20Techniques","dc:title":"Two-Hybrid System Techniques"},{"@id":"https://cir.nii.ac.jp/all?q=Ubiquitin-Conjugating%20Enzymes","dc:title":"Ubiquitin-Conjugating Enzymes"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Ubiquitins","dc:title":"Ubiquitins"},{"@id":"https://cir.nii.ac.jp/all?q=Cells,%20Cultured","dc:title":"Cells, Cultured"},{"@id":"https://cir.nii.ac.jp/all?q=Protein%20Binding","dc:title":"Protein Binding"}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050012570391407104","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"MicroRNA-101 Regulates 6-Hydroxydopamine-Induced Cell Death by Targeting Suppressor/Enhancer Lin-12-Like in SH-SY5Y Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1050299771254995456","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"輝け次代の担い手たち　神経変性疾患における蛋白輸送系の破綻と神経細胞死"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002217561565312","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Parkin interacts with Klokin1 for mitochondrial import and maintenance of membrane potential"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002219449586816","@type":"Article","resourceType":"学術雑誌論文(journal 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Disease"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567186891517184","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Endoplasmic Reticulum Stress and Apoptosis Contribute to the Pathogenesis of Dominantly Inherited Isolated GH Deficiency Due to GH1 Gene Splice Site Mutations"}]},{"@id":"https://cir.nii.ac.jp/crid/1360570166683582208","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"The\n            <i>parkin-coregulated gene</i>\n            product PACRG promotes TNF signaling by stabilizing LUBAC"}]},{"@id":"https://cir.nii.ac.jp/crid/1360572092750477952","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Prosaposin and its receptors GRP37 and GPR37L1 show increased immunoreactivity in the facial nucleus following facial nerve transection"}]},{"@id":"https://cir.nii.ac.jp/crid/1360846646079496448","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Mitochondrial Regulation by PINK1-Parkin Signaling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848657321217920","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Endoplasmic reticulum stress inducers provide protection against 6-hydroxydopamine-induced cytotoxicity"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848660497936256","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Deletion of Herp facilitates degradation of cytosolic proteins"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848662808214272","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Can parkin be a target for future treatment of Parkinson's disease?"}]},{"@id":"https://cir.nii.ac.jp/crid/1361131421912414976","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Decreased Activity of the Ghrhr and Gh Promoters Causes Dominantly Inherited GH Deficiency in Humanized GH1 Mouse Models"}]},{"@id":"https://cir.nii.ac.jp/crid/1361975841995622656","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Immunoreactivity of a G protein-coupled l-DOPA receptor GPR143, in Lewy bodies"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001204272093184","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Current studies on neuronal death and neurodegenerative diseases"},{"@language":"ja","@value":"神経細胞死と神経変性疾患の最先端研究"},{"@language":"ja-Kana","@value":"シンケイ サイボウシ ト シンケイ ヘンセイ シッカン ノ サイセンタン ケンキュウ"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001204273113984","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Neurodegeneration caused by ER stress?-The pathogenetic mechanisms underlying AR-JP."},{"@language":"ja","@value":"小胞体ストレスによる神経変性の分子機構―ＡＲ‐ＪＰのメカニズム―"},{"@value":"小胞体ストレスによる神経変性の分子機構--AR-JPのメカニズム"},{"@language":"ja-Kana","@value":"ショウホウタイ ストレス ニ ヨル シンケイ ヘンセイ ノ ブンシ キコウ AR JP ノ メカニズム"},{"@value":"Neurodegeneration caused by ER stress?"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001204627637248","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Antiparkinsonian Drugs and Their Neuroprotective Effects."}]},{"@id":"https://cir.nii.ac.jp/crid/1390001204631878656","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Possible Involvement of Ubiquitin Ligase HRD1 Insolubilization in Amyloid .BETA. Generation"},{"@value":"Possible Involvement of Ubiquitin Ligase HRD1 Insolubilization in Amyloid β Generation"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205025037440","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@value":"老化メカニズムの解明と老化制御の最前線　　２．Ｐａｒｋｉｎ蛋白質とパーキンソン病の発症メカニズム"},{"@language":"en","@value":"Parkin protein and molecular mechanism of Parkinson's disease"},{"@language":"ja-Kana","@value":"Parkin タンパクシツ ト パーキンソンビョウ ノ ハッショウ メカニズム"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205034672256","@type":"Article","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Recent progress and future direction of neurodegenerative disease research"},{"@language":"ja","@value":"シンポジウム２‐１　神経変性疾患研究の焦点‐新たな病的因子の登場と臨床への展望‐　基調講演：神経変性疾患研究の課題"},{"@value":"基調講演 神経変性疾患研究の課題"},{"@language":"ja-Kana","@value":"キチョウ コウエン シンケイ ヘンセイ シッカン ケンキュウ ノ 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