Tuong Huynh
Research associate at Baylor College of Medicine in Houston and co-author on a long run of papers from Andrea Ballabio's group on TFEB, the master switch for lysosome and autophagy genes, including the work that tied TFEB to mTOR, starvation and fat metabolism
Research Associate, Department of Molecular and Human Genetics, Baylor College of Medicine (Zoghbi Lab) · co-author with the Ballabio, Settembre and Sardiello groups (2011–2026)
Cells keep themselves clean with lysosomes, small acid-filled bags that break down worn-out parts, and with autophagy, the process that delivers those parts to the lysosome. In 2011 Carmine Settembre, Andrea Ballabio and colleagues, with Tuong Huynh among the co-authors, showed that one transcription factor, TFEB, switches on a whole programme of autophagy and lysosome genes when cells are starved (SET2011). In that first paper TFEB was controlled by the kinase ERK2. The 2012 follow-up (SET2012) found the link to mTORC1, the growth-control complex that sits on the lysosome surface: when nutrients are plentiful, mTORC1 phosphorylates TFEB and keeps it out of the nucleus, so the lysosome itself reports its state to the genes that build it.
The 2013 paper (SET2013) moved into living mice. Fasting switched on the TFEB gene in liver, muscle and kidney, and TFEB then boosted its own production in a feed-forward loop. In the liver it drove fat breakdown largely through PGC-1alpha and PPARalpha, and extra liver TFEB protected mice from diet-induced obesity. The most recent paper (FER2026) used kidney-specific mouse models to separate mTORC1 activity from TFEB/TFE3 activity and found that overactive mTORC1, not TFEB/TFE3 alone, is the main driver of kidney cysts and tumours in models of Birt-Hogg-Dube syndrome and tuberous sclerosis complex.
PubMed lists Tuong Huynh on about a dozen TFEB, lysosome and autophagy papers with the Ballabio, Settembre or Sardiello groups between 2011 and 2026. The early papers give no affiliation for this author; a 2020 paper and the 2026 kidney paper place Huynh at the Department of Molecular and Human Genetics, Baylor College of Medicine, and the Jan and Dan Duncan Neurological Research Institute of Texas Children's Hospital in Houston, where Ballabio's US laboratory is based. The Baylor College of Medicine staff directory lists Tuong B. Huynh as a Research Associate in the Department of Molecular and Human Genetics, attached to the Zoghbi Lab.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | TFEB links autophagy to lysosomal biogenesis SET2011 Co-author on the discovery that TFEB coordinates autophagy and lysosome genes during starvation. |
| 2012 | M | A lysosome-to-nucleus signalling mechanism senses and regulates the lysosome via mTOR and TFEB SET2012 Co-author on the paper showing that mTOR-dependent phosphorylation of TFEB lets the lysosome signal its own state to the nucleus. |
| 2013 | A | TFEB controls cellular lipid metabolism through a starvation-induced autoregulatory loop SET2013 Co-author on the mouse study showing that fasting turns on TFEB, which then drives its own gene and liver fat breakdown. |
| 2026 | A | Synergistic role of TFEB/TFE3 and mTORC1 in kidney cystogenesis and tumorigenesis FER2026 Co-author on the kidney mouse models that identified mTORC1 overactivity as the main driver of cysts and tumours, with TFEB/TFE3 adding to it. |
Co-authors in the Atlas 7
People with a profile here who share at least one study with Tuong Huynh.
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- Andrea Ballabio 4 shared studies Discovered that the transcription factor TFEB is a master switch for building lysosomes (SAR2009) and for autophagy. His lab was one of the groups that showed in 2012 that mTORC1 keeps TFEB out of the nucleus from the lysosome surface, and later (2020) that constitutive TFEB activation drives the kidney disease of Birt-Hogg-Dubé syndrome
- Carmine Settembre 3 shared studies Showed, as first author in Andrea Ballabio's lab, that TFEB drives autophagy as well as lysosome production, and, in parallel with other groups, that mTORC1 phosphorylates TFEB at the lysosome to keep this program switched off when nutrients are plentiful
- Alessia Calcagnì TIGEM researcher on the TFEB/TFE3 side of mTORC1 signalling; co-author on the lysosomal stress route to TFEB activation and on mouse models separating mTORC1 from TFEB/TFE3 in kidney cysts and tumours.
- David M. Sabatini Identified mTOR (as RAFT1) in 1994. His lab then mapped much of the machinery around it: raptor and rictor at the core of mTORC1 and mTORC2, the Rag–Ragulator system that docks mTORC1 on the lysosome, and the sensors that detect leucine, arginine and SAM
- Diego L. Medina Cell biologist at the Telethon Institute of Genetics and Medicine in Naples who showed how TFEB, the master switch for lysosome genes, is controlled by calcium released from lysosomes, and who works on lysosomal storage diseases
- Marco Ferniani First author of the study showing mTORC1 hyperactivation, not TFEB/TFE3 activity itself, is the primary driver of kidney cystogenesis and tumorigenesis in mouse models of Birt-Hogg-Dubé and Tuberous Sclerosis
- Roberto Zoncu Showed as a postdoc that mTORC1 senses amino acids from inside the lysosome, through the v-ATPase and Ragulator. His Berkeley lab has since mapped how the Rag GTPases and the folliculin complex switch mTORC1 on, and how lysosomal cholesterol feeds into the same system
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