WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7150

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  • Article
    Citation - WoS: 4
    Citation - Scopus: 4
    Autophagic Flux Is Impaired in the Brain Tissue of Tay-Sachs Disease Mouse Model
    (Public Library of Science, 2023) Şengül, Tuğçe; Can, Melike; Ateş, Nurselin; Seyrantepe, Volkan
    Tay-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.
  • Erratum
    Correction To: Excessive Replacement Changes Drive Evolution of Global Sheep Prion Protein (prnp) Sequences (heredity, (2022), 128, 5, (377-385), 10.1038/S41437-022-00520-6)
    (Springer, 2023) Teferedegn, Eden Yitna; Yaman, Yalçın; Sezgin, Efe; Ün, Cemal
    In this article the affiliation details for Author Cemal Ün were incorrectly given as Armauer Hansen research institute, Biotechnology and Bioinformatic Directorate, Addis Ababa, Ethiopia but should have been Department of Biology, Molecular Biology Division, Ege University, Izmir, Turkey. The original article has been corrected. © 2022, The Author(s), under exclusive licence to The Genetics Society.