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Jose A. Martina

Researcher at National Institutes of Health

Publications -  54
Citations -  6597

Jose A. Martina is an academic researcher from National Institutes of Health. The author has contributed to research in topics: TFEB & Golgi apparatus. The author has an hindex of 32, co-authored 50 publications receiving 4677 citations. Previous affiliations of Jose A. Martina include National University of Cordoba.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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MTORC1 functions as a transcriptional regulator of autophagy by preventing nuclear transport of TFEB

TL;DR: It is shown that MTORC1 regulates nuclear localization and activity of the transcription factor EB (TFEB), a member of the bHLH leucine-zipper family of transcription factors that drives expression of autophagy and lysosomal genes.
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Transcriptional Activation of Lysosomal Exocytosis Promotes Cellular Clearance

TL;DR: Induction of lysosomal exocytosis by TFEB overexpression rescued pathologic storage and restored normal cellular morphology both in vitro and in vivo in lysOSomal storage diseases (LSDs).
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The Nutrient-Responsive Transcription Factor TFE3 Promotes Autophagy, Lysosomal Biogenesis, and Clearance of Cellular Debris

TL;DR: The identification of transcription factor E3 (TFE3) as another regulator of lysosomal homeostasis that induced expression of genes encoding proteins involved in autophagy and lYSosomal biogenesis in ARPE-19 cells in response to starvation and lysOSomal stress is reported.
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Rag GTPases mediate amino acid–dependent recruitment of TFEB and MITF to lysosomes

TL;DR: Active Rag GTPases are required for recruitment of TFEB to lysosomes and its phosphorylation by mTORC1, inhibiting its function under nutrient-rich conditions.