Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/13389
Full metadata record
DC FieldValueLanguage
dc.contributor.authorŞengül, Tuğçe-
dc.contributor.authorCan, Melike-
dc.contributor.authorAteş, Nurselin-
dc.contributor.authorSeyrantepe, Volkan-
dc.date.accessioned2023-04-19T12:39:44Z-
dc.date.available2023-04-19T12:39:44Z-
dc.date.issued2023-
dc.identifier.issn1932-6203-
dc.identifier.urihttps://doi.org/10.1371/journal.pone.0280650-
dc.identifier.urihttps://hdl.handle.net/11147/13389-
dc.description.abstractTay-Sachs disease is a lethal lysosomal storage disorder caused by mutations in the HexA gene encoding the α subunit of the lysosomal β-hexosaminidase enzyme (HEXA). Abnormal GM2 ganglioside accumulation causes progressive deterioration in the central nervous system in Tay-Sachs patients. Hexa-/-mouse model failed to display abnormal phenotype. Recently, our group generated Hexa-/-Neu3-/-mouse showed severe neuropathological indications similar to Tay-Sachs patients. Despite excessive GM2 ganglioside accumulation in the brain and visceral organs, the regulation of autophagy has not been clarified yet in the Tay-Sachs disease mouse model. Therefore, we investigated distinct steps of autophagic flux using markers including LC3 and p62 in four different brain regions from the Hexa-/-Neu3-/-mice model of Tay-Sachs disease. Our data revealed accumulated autophagosomes and autophagolysosomes indicating impairment in autophagic flux in the brain. We suggest that autophagy might be a new therapeutic target for the treatment of devastating Tay-Sachs disease. © 2023 Sengul et al.en_US
dc.description.sponsorshipFunding: This study is funded by TUBİTAK Grant No:215Z083en_US
dc.language.isoenen_US
dc.publisherPublic Library of Scienceen_US
dc.relationErken Başlangıçlı Tay-Sachs Hastalığı Fare Modelinde Hücresel Patolojinin Araştırılmasıtr
dc.relation.ispartofPLoS ONEen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectBeta-N-Acetylhexosaminidasesen_US
dc.subjectGangliosidesen_US
dc.subjectAnimalsen_US
dc.subjectAutophagyen_US
dc.subjectBrainen_US
dc.subjectTay-Sachs diseaseen_US
dc.titleAutophagic flux is impaired in the brain tissue of Tay-Sachs disease mouse modelen_US
dc.typeArticleen_US
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.identifier.volume18en_US
dc.identifier.issue3 Marchen_US
dc.identifier.wosWOS:000985134400073en_US
dc.identifier.scopus2-s2.0-85150230228en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1371/journal.pone.0280650-
dc.identifier.pmid36928510en_US
dc.relation.grantno215Z083-
dc.authorscopusid57856462600-
dc.authorscopusid57855836700-
dc.authorscopusid57195980858-
dc.authorscopusid6602725956-
dc.identifier.wosqualityQ2-
dc.identifier.scopusqualityQ1-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.openairetypeArticle-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
Files in This Item:
File SizeFormat 
Autophagic-flux.pdf2.67 MBAdobe PDFView/Open
Show simple item record



CORE Recommender

SCOPUSTM   
Citations

1
checked on Nov 29, 2024

WEB OF SCIENCETM
Citations

1
checked on Nov 23, 2024

Page view(s)

222
checked on Dec 2, 2024

Download(s)

50
checked on Dec 2, 2024

Google ScholarTM

Check




Altmetric


Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.