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Szabolcs Takáts

Researcher at Eötvös Loránd University

Publications -  24
Citations -  6690

Szabolcs Takáts is an academic researcher from Eötvös Loránd University. The author has contributed to research in topics: Autophagy & Autophagosome. The author has an hindex of 15, co-authored 24 publications receiving 5970 citations. Previous affiliations of Szabolcs Takáts include Hungarian Academy of Sciences & University of Texas Southwestern Medical Center.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Autophagosomal Syntaxin17-dependent lysosomal degradation maintains neuronal function in Drosophila

Szabolcs Takáts, +8 more
- 13 May 2013 - 
TL;DR: Lysosomal degradation and recycling of sequestered autophagosome content is crucial to maintain proper functioning of the fly nervous system.
Journal ArticleDOI

Interaction of the HOPS complex with Syntaxin 17 mediates autophagosome clearance in Drosophila

Szabolcs Takáts, +9 more
- 15 Apr 2014 - 
TL;DR: Interaction of the autophagosomal SNARE Syntaxin 17 (Syx17) with the homotypic fusion and vacuole protein–sorting (HOPS) tethering complex is necessary for the fusion of Autophagosomes with lysosomes.
Journal ArticleDOI

Mutation in ATG5 reduces autophagy and leads to ataxia with developmental delay.

Myungjin Kim, +23 more
- 26 Jan 2016 - 
TL;DR: The identified a homozygous missense mutation, changing a conserved amino acid, in ATG5 in two siblings with congenital ataxia, mental retardation, and developmental delay are identified, demonstrating the critical role of autophagy in preventing neurological diseases and maintaining neuronal health.
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The Ccz1-Mon1-Rab7 module and Rab5 control distinct steps of autophagy.

Krisztina Hegedűs, +7 more
- 15 Oct 2016 - 
TL;DR: The endocytic Rab5 effectors Ccz1-Mon1 complex and Rab7 promote autophagosome-lysosome fusion independent of Rab5, which facilitates a later step of autophagy: degradation of cargo within lysosomes.