Vito Porcelli

TL;DR: Excessive Ca2+ levels are responsible for boosting AGC activity, mitochondrial metabolism and, to a more variable degree, oxidative stress in autistic brains, and their modulation could provide new preventive and therapeutic strategies.

TL;DR: In this review the state-of-the-art of computational approaches in 3D protein comparative modeling and in the study of protein-ligand interactions is provided and a possible combined/concerted multistep strategy for protein function prediction is described.

TL;DR: It is demonstrated that, in the absence of glucose, activated macrophages increase CIC acetylation to enhance citrate efflux from mitochondria not only to produce inflammatory mediators but also to meet the NADPH demand through the actions of isocitrate dehydrogenase and malic enzyme.

TL;DR: This carrier catalyzed substantial uniport besides a counter-exchange transport, exhibited a high transport affinity for arginine and lysine, and was saturable and inhibited by mercurial compounds and other inhibitors of mitochondrial carriers to various degrees.

TL;DR: It is hypothesized that the neuromuscular junction impairment may be related to pre-synaptic nerve terminal abnormalities, and the findings highlight the complex machinery required to ensure efficient neuromUScular function, beyond the proteomes exclusive to the neurmuscular synapse.