Jing Zhou
Researcher in Luis Parada's lab whose work includes the 2009 study showing that rapamycin prevents and reverses brain abnormalities in neural Pten-knockout mice
UT Southwestern Medical Center, Parada lab · Pten/mTORC1 neurodevelopmental biology, 2005–2013
Jing Zhou was a fixture of Luis F. Parada's lab at UT Southwestern for roughly eight years (2005-2013), co-authoring a remarkable run of the lab's flagship papers on PTEN and mTORC1 signaling in the nervous system — across Neuron, Genes & Development, the Journal of Neuroscience, Nature Cell Biology, Human Molecular Genetics and PNAS. The 2009 J Neurosci paper in this Atlas entry showed that pharmacological inhibition of mTORC1 (rapamycin) suppressed anatomical, cellular, and behavioral abnormalities caused by neural Pten deletion in mice — evidence that mTORC1 hyperactivity underlies the neuronal hypertrophy and part of the behavioural phenotype, and a rationale for mTOR inhibitors in PTEN-related neurodevelopmental disorders.
The breadth of this authorship across the lab's genetic mouse models suggests a long-term research scientist role. The PubMed trail under the name 'Jing Zhou' effectively ends with a 2013 PNAS paper; given how common this name is, the later career could not be reliably traced.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2009 | A | Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice ZHO2009 First author of the paper showing pharmacological mTORC1 inhibition (rapamycin) reverses anatomical, cellular, and behavioral abnormalities in neural Pten-knockout mice. |
Co-authors in the Atlas 1
People with a profile here who share at least one study with Jing Zhou.
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- Luis F. Parada Uses genetically engineered mouse models to study nervous system tumours such as glioblastoma and neurofibromatosis-related tumours, and the brain effects of PTEN loss.
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