Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.
Epsin has a key role in the coupling of actin to endocytic clathrin coated pits that is required for their maturation and helps capture SNAREs at endocytic clathrin coated pits.
Imaging with electron microscopy and cryo-electron tomography reveals that competition between Cdc42 and Gic1 for the same subunit within septins controls the formation and breakdown of septin filaments.
Mature myelin sheaths are scaffolded by the anillin-dependent assembly of septin filaments, thereby facilitating rapid nerve conduction in the healthy CNS.
The recently characterized opsin group of xenopsins is likely a major player in animal eye evolution and may have been present in an ancient, highly plastic eye photoreceptor cell type.
A rigorous and transparent evaluation of mesenchymal stem cell therapy for sepsis suggests it may be efficacious, although the strength of these findings is tempered by threats to validity in the studies that were included.
A subset of hypothalamic POMC neurons that express leptin receptors control metabolic responses to changing energy availability including regulating blood glucose and leptin levels.
Autocrine activation of macrophages is modulated by Connexin-43-mediated ATP release in response to TLR-4 and -2 agonists in a P2Y1-dependent manner, ultimately determining sepsis survival.
Leptin acts in the paraventricular nucleus to slowly increase sympathetic nerve activity to skeletal muscle and brown adipose tissue via induction of its own receptor in TRH glutamatergic neurons.
