DYRK1A, a kinase associated with intellectual developmental disorders and organ growth regulation, functions in cell growth by promoting mTORC1 activity.

Tsc2 inactivation in mouse mesenchymal progenitors produced tumors with vascular anomalies reminiscent of human angiomyolipomas, and a gene expression signature in Tsc2-deficient tissues which included Lgals3, as a novel potential biomarker for TSC1/2 loss.

Tsc1 mutation in cerebellar Purkinje cells leads to downregulation of synapse genes that are targets of the Fragile X Mental Retardation Protein.

The key Target of Rapamycin Complex (TORC1) component Kog1 moves into bodies during glucose starvation to limit reactivation of the complex.

Genetics and biochemical analyses reveal an evolutionarily conserved mechanism to regulate gene isoform expression by mTORC1 and implicate possible gene isoform imbalance in cancer and neurological disorders with mTORC1 pathway dysregulation.

Label-free three-photon imaging of whole, uncleared intact organoids generated from Rett syndrome patients show shorter migration distances and slower migration speeds of mutant radially migrating neurons with more tortuous trajectories.

Comprehensive mouse genetic analyses show, by having mTORC1 constitutively active, a RPC divides and exhausts mitotic capacity faster than neighboring RPCs, and thus produces retinal cells that degenerate with aging-related changes in the mature mouse retina.

ATF4 is a metabolic effector of mTORC1 signaling, co-opted to induce gene targets involved in amino acid synthesis, uptake, and tRNA charging, contributing to mTORC1-driven protein and glutathione synthesis.

mTOR signaling regulates the morphology of a human-enriched neural stem cell population and thus contributes to the radial architecture of the developing human cortex with implications for neurodevelopmental disease.

Brain lactate and pH changes, identified as common features in diverse neuropsychiatric animal models, may represent transdiagnostic endophenotypes associated with cognitive impairment.