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CiNii Research
Paeoniflorin eliminates a mutant AR via NF-YA-dependent proteolysis in spinal and bulbar muscular atrophy
- 資料種別
- 記事
- 著者
- Genki Tohnaiほか
- 出版者
- Oxford University Press (OUP)
- 出版年
- 2014-02-18
- 資料形態
- デジタル
- 掲載誌名
- Human Molecular Genetics 23 13
- 掲載ページ
- p.3552-3565
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デジタル
- 資料種別
- 記事
- 著者標目
- 出版年月日等
- 2014-02-18
- 出版年(W3CDTF)
- 2014-02-18
- タイトル(掲載誌)
- Human Molecular Genetics
- 巻号年月日等(掲載誌)
- 23 13
- 掲載巻
- 23
- 掲載号
- 13
- 掲載ページ
- 3552-3565
- 掲載年月日(W3CDTF)
- 2014-02-18
- ISSN(掲載誌)
- 09646906
- 出版事項(掲載誌)
- Oxford University Press (OUP)
- 対象利用者
- 一般
- DOI
- 10.1093/hmg/ddu066
- 作成日(W3CDTF)
- 2014-02-19
- オンライン閲覧公開範囲
- インターネット公開
- 参照
- Potential therapeutic targets in polyglutamine-mediated diseasesOverexpression of hepatocyte growth factor in SBMA model mice has an additive effect on combination therapy with castrationBIIB021, a synthetic Hsp90 inhibitor, induces mutant ataxin-1 degradation through the activation of heat shock factor 1Protein Misfolding and Aggregation as a Therapeutic Target for Polyglutamine Diseasesオートファジー活性化天然化合物による神経変性疾患の治療哺乳類HSP40の発見の経緯とその後の進展
- 参照
- Heat shock factor-1 influences pathological lesion distribution of polyglutamine-induced neurodegenerationInsulinlike Growth Factor (IGF)-1 Administration Ameliorates Disease Manifestations in a Mouse Model of Spinal and Bulbar Muscular Atrophyp62/SQSTM1 Differentially Removes the Toxic Mutant Androgen Receptor via Autophagy and Inclusion Formation in a Spinal and Bulbar Muscular Atrophy Mouse ModelThe pathogenic mechanisms of polyglutamine diseases and current therapeutic strategiesTestosterone Reduction Prevents Phenotypic Expression in a Transgenic Mouse Model of Spinal and Bulbar Muscular AtrophyActivation of Hsp70 reduces neurotoxicity by promoting polyglutamine protein degradationCHIP is a chaperone‐dependent E3 ligase that ubiquitylates unfolded proteinLC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processingLeuprorelin rescues polyglutamine-dependent phenotypes in a transgenic mouse model of spinal and bulbar muscular atrophyHsp40 Gene Therapy Exerts Therapeutic Effects on Polyglutamine Disease Mice via a Non-Cell Autonomous MechanismRole of the CCAAT-Binding Protein NFY in SCA17 PathogenesisPathogenesis and molecular targeted therapy of spinal and bulbar muscular atrophyViral delivery of miR-196a ameliorates the SBMA phenotype via the silencing of CELF2Disrupted Transforming Growth Factor-β Signaling in Spinal and Bulbar Muscular AtrophyMolecular chaperones enhance the degradation of expanded polyglutamine repeat androgen receptor in a cellular model of spinal and bulbar muscular atrophyWidespread nuclear and cytoplasmic accumulation of mutant androgen receptor in SBMA patientsCHIP participates in protein triage decisions by preferentially ubiquitinating Hsp70‐bound substratesTranscriptional activation of TFEB/ZKSCAN3 target genes underlies enhanced autophagy in spinobulbar muscular atrophyTFEB regulates lysosomal proteostasisCHIP Overexpression Reduces Mutant Androgen Receptor Protein and Ameliorates Phenotypes of the Spinal and Bulbar Muscular Atrophy Transgenic Mouse ModelTherapeutics development for triplet repeat expansion diseasesPaeoniflorin, a novel heat shock protein–inducing compoundNeurotoxic protein oligomerisation associated with polyglutamine diseasesCo-induction of the heat shock response ameliorates disease progression in a mouse model of human spinal and bulbar muscular atrophy: implications for therapyClinical features of spinal and bulbar muscular atrophyNeurotoxic effects of androgens in spinal and bulbar muscular atrophyMutant Huntingtin reduces HSP70 expression through the sequestration of NF-Y transcription factorA Gene Network Regulating Lysosomal Biogenesis and FunctionTranscriptional Activation of Lysosomal Exocytosis Promotes Cellular ClearanceNF-Y and the transcriptional activation of CCAAT promotersMolecular Pathogenesis of Protein Misfolding Diseases: Pathological Molecular Environments Versus Quality Control Systems Against Misfolded ProteinsAltered chromatin architecture underlies progressive impairment of the heat shock response in mouse models of Huntington diseaseHeat shock proteins in neurodegenerative diseases: Pathogenic roles and therapeutic implicationsOver-expression of inducible HSP70 chaperone suppresses neuropathology and improves motor function in SCA1 miceCytoplasmic retention of polyglutamine-expanded androgen receptor ameliorates disease via autophagy in a mouse model of spinal and bulbar muscular atrophyTFEB Links Autophagy to Lysosomal BiogenesisProtein Quality Control in the Cytosol and the Endoplasmic Reticulum: Brothers in ArmsASC-J9 ameliorates spinal and bulbar muscular atrophy phenotype via degradation of androgen receptorASICs mediate the modulatory effect by paeoniflorin on alpha-synuclein autophagic degradationTransgenic mice with an expanded CAG repeat controlled by the human AR promoter show polyglutamine nuclear inclusions and neuronal dysfunction without neuronal cell deathSpinal and bulbar muscular atrophy: Skeletal muscle pathology in male patients and heterozygous femalesNatural history of spinal and bulbar muscular atrophy (SBMA): a study of 223 Japanese patients17-AAG, an Hsp90 inhibitor, ameliorates polyglutamine-mediated motor neuron degenerationHeat Shock Protein 70 Chaperone Overexpression Ameliorates Phenotypes of the Spinal and Bulbar Muscular Atrophy Transgenic Mouse Model by Reducing Nuclear-Localized Mutant Androgen Receptor ProteinPGC-1α Rescues Huntington’s Disease Proteotoxicity by Preventing Oxidative Stress and Promoting TFEB FunctionAltered transcriptional regulation in cells expressing the expanded polyglutamine androgen receptorNeuronal expression of TATA box-binding protein containing expanded polyglutamine in knock-in mice reduces chaperone protein response by impairing the function of nuclear factor-Y transcription factorEfficacy and safety of dutasteride in patients with spinal and bulbar muscular atrophy: a randomised placebo-controlled trialThe Induction Levels of Heat Shock Protein 70 Differentiate the Vulnerabilities to Mutant Huntingtin among Neuronal SubtypesGlycogen Synthase Kinase 3 Inhibition Promotes Lysosomal Biogenesis and Autophagic Degradation of the Amyloid-β Precursor ProteinCHIP Suppresses Polyglutamine Aggregation and Toxicity<i>In Vitro</i>and<i>In Vivo</i>X-LINKED RECESSIVE BULBOSPINAL NEURONOPATHYEfficacy and safety of leuprorelin in patients with spinal and bulbar muscular atrophy (JASMITT study): a multicentre, randomised, double-blind, placebo-controlled trialSuppression of protein aggregation by chaperone modification of high molecular weight complexesProteostasis and neurodegeneration: the roles of proteasomal degradation and autophagy
- 連携機関・データベース
- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
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