NIH R01 · 2025
Establishing the Function of TMEM184B in mTORC1 Regulation and Synaptic Maintenance
Synaptic disruption is a prelude to and often a primary cause of neurological disease, but we have few strategies to correct dysmorphic synapses, even if they occur early in the degenerative process. Growth control pathways, i.e. those that promote protein and lipid synthesis while reducing catabolism, regulate synaptic form that in turn ensures efficient function and plasticity. The 7-pass endosomal membrane protein TMEM184B regulates synaptic structure and function across species; accordingly, its loss causes exuberant synaptic sprouting, swollen nerve terminals, and altered excitability. In humans, disruption of conserved amino acids in TMEM184B is linked to nervous system disruptions…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.