Acetylcholine, a common modulator in the brain, controls spike-frequency adaptation by specifically attenuating Ether-a-go-go related K+ currents, thereby explaining many cortical network statistical changes often observed in vivo.
The multi-stage model of carcinogenesis requires the incorporation of aging-dependent somatic selection and life history-dependent evolution of species-specific tumor suppressor mechanisms in order to generalize carcinogenesis across tissues and species.
Endothelial tightening by augmenting low level Wnt/β-catenin activity in vessels of the mouse subfornical organ, influences neuronal activation in water-deprived mice, linking endothelial barrier properties to neuro-vascular coupling.
In mouse models of Huntington's disease, striatal spiny projection neurons up-regulate dendritic potassium channels, which impairs their normal function, but a zinc finger gene therapy can reverse this deficit.
A near-complete flux balance analysis model of a minimal cell demonstrates the high essentiality of its metabolic genes, agrees well with experimental essentiality data and suggests some further gene removals.
Mitogen-activated protein kinase phosphatase 1 (DUSP1) deficiency causes early redox imbalance and increased inflammatory response in the cochlea, leading to cell loss and progressive neurosensory hearing loss.