000166690 001__ 166690
000166690 005__ 20240229133527.0
000166690 0247_ $$2doi$$a10.1080/15548627.2020.1871211
000166690 0247_ $$2pmid$$apmid:33404278
000166690 0247_ $$2ISSN$$a1554-8627
000166690 0247_ $$2ISSN$$a1554-8635
000166690 0247_ $$2altmetric$$aaltmetric:97259225
000166690 037__ $$aDKFZ-2021-00043
000166690 041__ $$aeng
000166690 082__ $$a570
000166690 1001_ $$aZhu, Jun-Yi$$b0
000166690 245__ $$aAutophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperone Hsc70-5 in Drosophila.
000166690 260__ $$aAbingdon, Oxon$$bTaylor & Francis$$c2021
000166690 3367_ $$2DRIVER$$aarticle
000166690 3367_ $$2DataCite$$aOutput Types/Journal article
000166690 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1634295091_1826
000166690 3367_ $$2BibTeX$$aARTICLE
000166690 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000166690 3367_ $$00$$2EndNote$$aJournal Article
000166690 500__ $$a#LA:B180# /2021 Oct;17(10):3160-3174
000166690 520__ $$aWe investigated in larval and adult Drosophila models whether loss of the mitochondrial chaperone Hsc70-5 is sufficient to cause pathological alterations commonly observed in Parkinson disease. At affected larval neuromuscular junctions, no effects on terminal size, bouton size or number, synapse size, or number were observed, suggesting that we studied an early stage of pathogenesis. At this stage, we noted a loss of synaptic vesicle proteins and active zone components, delayed synapse maturation, reduced evoked and spontaneous excitatory junctional potentials, increased synaptic fatigue, and cytoskeleton rearrangements. The adult model displayed ATP depletion, altered body posture, and susceptibility to heat-induced paralysis. Adult phenotypes could be suppressed by knockdown of dj-1β, Lrrk, DCTN2-p50, DCTN1-p150, Atg1, Atg101, Atg5, Atg7, and Atg12. The knockdown of components of the macroautophagy/autophagy machinery or overexpression of human HSPA9 broadly rescued larval and adult phenotypes, while disease-associated HSPA9 variants did not. Overexpression of Pink1 or promotion of autophagy exacerbated defects.
000166690 536__ $$0G:(DE-HGF)POF4-312$$a312 - Funktionelle und strukturelle Genomforschung (POF4-312)$$cPOF4-312$$fPOF IV$$x0
000166690 588__ $$aDataset connected to CrossRef, PubMed,
000166690 650_7 $$2Other$$a Atg1
000166690 650_7 $$2Other$$a Hsc70-5
000166690 650_7 $$2Other$$amicrotubule
000166690 650_7 $$2Other$$amitochondria
000166690 650_7 $$2Other$$amitophagy
000166690 650_7 $$2Other$$arapamycin
000166690 650_7 $$2Other$$asynapse
000166690 7001_ $$0P:(DE-He78)77839d5cf53d09e62bdfca3d3172fab1$$aHannan, Shabab Bin$$b1
000166690 7001_ $$0P:(DE-He78)44dc011368b331679dbc8d341ae41420$$aDräger, Nina$$b2
000166690 7001_ $$aVereshchagina, Natalia$$b3
000166690 7001_ $$aKrahl, Ann-Christin$$b4
000166690 7001_ $$aFu, Yulong$$b5
000166690 7001_ $$aElliott, Christopher J H$$b6
000166690 7001_ $$aHan, Zhe$$b7
000166690 7001_ $$0P:(DE-He78)813a306749dc9a24333a77867a42bbd9$$aJahn, Thomas$$b8
000166690 7001_ $$0P:(DE-He78)e9a603e8a132f8501ed78cf4995c246c$$aRasse, Tobias$$b9$$eLast author
000166690 773__ $$0PERI:(DE-600)2262043-6$$a10.1080/15548627.2020.1871211$$gp. 15548627.2020.1871211$$n10$$p3160-3174$$tAutophagy$$v17$$x1554-8635$$y2021
000166690 909CO $$ooai:inrepo02.dkfz.de:166690$$pVDB
000166690 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)77839d5cf53d09e62bdfca3d3172fab1$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
000166690 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)44dc011368b331679dbc8d341ae41420$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000166690 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)813a306749dc9a24333a77867a42bbd9$$aDeutsches Krebsforschungszentrum$$b8$$kDKFZ
000166690 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)e9a603e8a132f8501ed78cf4995c246c$$aDeutsches Krebsforschungszentrum$$b9$$kDKFZ
000166690 9131_ $$0G:(DE-HGF)POF4-312$$1G:(DE-HGF)POF4-310$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunktionelle und strukturelle Genomforschung$$x0
000166690 9130_ $$0G:(DE-HGF)POF3-312$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunctional and structural genomics$$x0
000166690 9141_ $$y2021
000166690 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bAUTOPHAGY : 2018$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2020-09-06
000166690 915__ $$0StatID:(DE-HGF)9910$$2StatID$$aIF >= 10$$bAUTOPHAGY : 2018$$d2020-09-06
000166690 9201_ $$0I:(DE-He78)B180-20160331$$kB180$$lProteostase neurodegenerativer Erkrankungen$$x0
000166690 980__ $$ajournal
000166690 980__ $$aVDB
000166690 980__ $$aI:(DE-He78)B180-20160331
000166690 980__ $$aUNRESTRICTED