Helen S. Bateup
Senior/corresponding author of a 2026 Nature study showing mTORC1 hyperactivity drives cell-autonomous astrocyte reactivity in tuberous sclerosis
Associate Professor of Molecular and Cell Biology & Neuroscience, University of California, Berkeley · Weill Neurohub Investigator · PhD, The Rockefeller University
Bateup Lab, UC Berkeley (Berkeley, California, USA) ↗ Lab lineagetrained under Bernardo L. Sabatini → ORCID0000-0002-0135-0972 ↗
Portrait: Bateup Lab, UC Berkeley
Helen Bateup directs a lab in UC Berkeley's Department of Molecular and Cell Biology studying how genetic mutations linked to epilepsy and autism — especially in the TSC1/TSC2–mTORC1 pathway — disrupt neural development, synaptic function and circuit excitability. She trained as a PhD student at The Rockefeller University and is a Weill Neurohub Investigator.
In this Atlas she is senior/corresponding author of a 2026 Nature study using human brain organoids grown for 9+ months (to replicate human developmental timelines) alongside resected tuber tissue from tuberous sclerosis patients. The work shows that TSC2 loss biases neural progenitors toward reactive, pro-inflammatory astrocytes in a cell-autonomous manner — independent of seizures — implicating glial dysfunction, not just neuronal hyperexcitability, as a driver of TSC pathology and a potential therapeutic target.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2013 | M | Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis BAT2013 First author showing that Tsc1 loss in mouse hippocampal neurons weakens their inhibitory input and drives network hyperexcitability and seizure susceptibility, which rapamycin normalised. |
| 2026 | M | mTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis LI2026C Senior/corresponding author demonstrating that mTORC1-hyperactive neural progenitors become pro-inflammatory reactive astrocytes in a cell-autonomous manner, independent of seizure activity — implicating glial dysfunction as a driver, not only a consequence, of TSC pathology. |
Co-authors in the Atlas 3
People with a profile here who share at least one study with Helen S. Bateup.
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- Bernardo L. Sabatini Neurobiologist who studies how synapses and circuits change during development and learning; his lab showed that loss of Tsc1 in mouse hippocampal neurons weakens inhibitory input and tips circuits toward hyperexcitability.
- Dirk Hockemeyer Stem-cell biologist whose laboratory builds engineered human stem-cell and mouse models of disease, using genome editing and functional genomics screens.
- Thomas L. Li Co-first author of a 2026 Nature study showing mTORC1 hyperactivity drives reactive astrocytes as a primary, seizure-independent consequence of TSC2 loss, implicating glial dysfunction as a driver of tuberous sclerosis pathology
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