000140217 001__ 140217
000140217 005__ 20240430145157.0
000140217 0247_ $$2doi$$a10.1016/j.nbd.2018.08.001
000140217 0247_ $$2pmid$$apmid:30092270
000140217 0247_ $$2ISSN$$a0969-9961
000140217 0247_ $$2ISSN$$a1095-953X
000140217 0247_ $$2altmetric$$aaltmetric:46641495
000140217 037__ $$aDZNE-2020-06539
000140217 041__ $$aEnglish
000140217 082__ $$a570
000140217 1001_ $$aPaiva, Isabel$$b0
000140217 245__ $$aAlpha-synuclein deregulates the expression of COL4A2 and impairs ER-Golgi function.
000140217 260__ $$aOrlando, Fla.$$bAcademic Press$$c2018
000140217 264_1 $$2Crossref$$3print$$bElsevier BV$$c2018-11-01
000140217 3367_ $$2DRIVER$$aarticle
000140217 3367_ $$2DataCite$$aOutput Types/Journal article
000140217 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1714481461_8224
000140217 3367_ $$2BibTeX$$aARTICLE
000140217 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000140217 3367_ $$00$$2EndNote$$aJournal Article
000140217 520__ $$aAlpha-synuclein (aSyn) is the major protein component of Lewy bodies and Lewy neurites, the typical pathological hallmarks in Parkinson's disease (PD) and Dementia with Lewy bodies. aSyn is capable of inducing transcriptional deregulation, but the precise effect of specific aSyn mutants associated with familial forms of PD, remains unclear. Here, we used transgenic mice overexpressing human wild-type (WT) or A30P aSyn to compare the transcriptional profiles of the two animal models. We found that A30P aSyn promotes strong transcriptional deregulation and increases DNA binding. Interestingly, COL4A2, a major component of basement membranes, was found to be upregulated in both A30P aSyn transgenic mice and in dopaminergic neurons expressing A30P aSyn, suggesting a crucial role for collagen related genes in aSyn-induced toxicity. Finally, we observed that A30P aSyn alters Golgi morphology and increases the susceptibility to endoplasmic reticulum (ER) stress in dopaminergic cells. In total, our findings provide novel insight into the putative role of aSyn on transcription and on the molecular mechanisms involved, thereby opening novel avenues for future therapeutic interventions in PD and other synucleinopathies.
000140217 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000140217 542__ $$2Crossref$$i2018-11-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000140217 588__ $$aDataset connected to CrossRef, PubMed,
000140217 650_7 $$2NLM Chemicals$$aCol4a2 protein, mouse
000140217 650_7 $$2NLM Chemicals$$aCollagen Type IV
000140217 650_7 $$2NLM Chemicals$$aPeptide Fragments
000140217 650_7 $$2NLM Chemicals$$aSnca protein, mouse
000140217 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000140217 650_2 $$2MeSH$$aAnimals
000140217 650_2 $$2MeSH$$aCells, Cultured
000140217 650_2 $$2MeSH$$aCollagen Type IV: biosynthesis
000140217 650_2 $$2MeSH$$aCollagen Type IV: genetics
000140217 650_2 $$2MeSH$$aEndoplasmic Reticulum: physiology
000140217 650_2 $$2MeSH$$aGene Expression
000140217 650_2 $$2MeSH$$aGolgi Apparatus: physiology
000140217 650_2 $$2MeSH$$aHumans
000140217 650_2 $$2MeSH$$aMice
000140217 650_2 $$2MeSH$$aMice, Inbred C57BL
000140217 650_2 $$2MeSH$$aMice, Transgenic
000140217 650_2 $$2MeSH$$aPeptide Fragments: biosynthesis
000140217 650_2 $$2MeSH$$aPeptide Fragments: genetics
000140217 650_2 $$2MeSH$$aalpha-Synuclein: biosynthesis
000140217 650_2 $$2MeSH$$aalpha-Synuclein: genetics
000140217 7001_ $$0P:(DE-2719)2811223$$aJain, Gaurav$$b1$$udzne
000140217 7001_ $$aLázaro, Diana F$$b2
000140217 7001_ $$aJerčić, Kristina Gotovac$$b3
000140217 7001_ $$aHentrich, Thomas$$b4
000140217 7001_ $$0P:(DE-2719)2812366$$aKerimoglu, Cemil$$b5$$udzne
000140217 7001_ $$aPinho, Raquel$$b6
000140217 7001_ $$aSzegő, Èva M$$b7
000140217 7001_ $$0P:(DE-2719)2810773$$aBurkhardt, Susanne$$b8$$udzne
000140217 7001_ $$0P:(DE-2719)2810626$$aCapece, Vincenzo$$b9$$udzne
000140217 7001_ $$0P:(DE-2719)2810512$$aHalder, Rashi$$b10$$udzne
000140217 7001_ $$0P:(DE-2719)2811643$$aIslam, Rezaul$$b11$$udzne
000140217 7001_ $$aXylaki, Mary$$b12
000140217 7001_ $$aCaldi Gomes, Lucas A$$b13
000140217 7001_ $$aRoser, Anna-Elisa$$b14
000140217 7001_ $$0P:(DE-HGF)0$$aLingor, Paul$$b15
000140217 7001_ $$aSchulze-Hentrich, Julia M$$b16
000140217 7001_ $$aBorovečki, Fran$$b17
000140217 7001_ $$0P:(DE-2719)2000047$$aFischer, André$$b18$$udzne
000140217 7001_ $$0P:(DE-HGF)0$$aOuteiro, Tiago F$$b19$$eCorresponding author
000140217 77318 $$2Crossref$$3journal-article$$a10.1016/j.nbd.2018.08.001$$b : Elsevier BV, 2018-11-01$$p121-135$$tNeurobiology of Disease$$v119$$x0969-9961$$y2018
000140217 773__ $$0PERI:(DE-600)1471408-5$$a10.1016/j.nbd.2018.08.001$$gVol. 119, p. 121 - 135$$p121-135$$q119<121 - 135$$tNeurobiology of disease$$v119$$x0969-9961$$y2018
000140217 8564_ $$uhttps://pub.dzne.de/record/140217/files/DZNE-2020-06539_Restricted.pdf
000140217 8564_ $$uhttps://pub.dzne.de/record/140217/files/DZNE-2020-06539_Restricted.pdf?subformat=pdfa$$xpdfa
000140217 909CO $$ooai:pub.dzne.de:140217$$pVDB
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811223$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b1$$kDZNE
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812366$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810773$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b8$$kDZNE
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810626$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b9$$kDZNE
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810512$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b10$$kDZNE
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811643$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b11$$kDZNE
000140217 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2000047$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b18$$kDZNE
000140217 9131_ $$0G:(DE-HGF)POF3-342$$1G:(DE-HGF)POF3-340$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lErkrankungen des Nervensystems$$vDisease Mechanisms and Model Systems$$x0
000140217 9141_ $$y2018
000140217 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bNEUROBIOL DIS : 2021$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2022-09-20T10:26:40Z
000140217 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2022-09-20T10:26:40Z
000140217 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Blind peer review$$d2022-09-20T10:26:40Z
000140217 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2022-11-18
000140217 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bNEUROBIOL DIS : 2021$$d2022-11-18
000140217 9201_ $$0I:(DE-2719)1410002$$kAG Fischer$$lEpigenetics and Systems Medicine in Neurodegenerative Diseases$$x0
000140217 9201_ $$0I:(DE-2719)1440012$$kAG Bonn 2$$lComputational Systems Biology$$x1
000140217 980__ $$ajournal
000140217 980__ $$aVDB
000140217 980__ $$aI:(DE-2719)1410002
000140217 980__ $$aI:(DE-2719)1440012
000140217 980__ $$aUNRESTRICTED