Michaela B.C. Kilander

TL;DR: WNT-5A emerges as an important means of astrocyte-microglia communication and is suggested as a new player in neuroinflammatory conditions, such as neurodegenerative disease, hypoxia, stroke, injury and infection.

TL;DR: The current understanding of those autism risk genes that affect the structural connectivity of neurons is discussed, and whether and how the neuronal structure and function are affected when these genes are mutated will provide insights toward developing effective interventions aimed at improving the lives of people with autism and their families.

TL;DR: The combined results show that FZD6 mutations can result in severe defects in nail and claw formation through reduced or abolished membranous FzD(6) levels and several nonfunctional WNT-FZD pathways.

TL;DR: G‐protein precoupling of FZD6 and WNT‐5A‐induced signaling to extracellular signal‐regulated kinase1/2 were impaired by DVL knockdown or overexpression, arguing for a strict dependence of F zD6‐G‐ Protein coupling on DVL levels and identifying DVL as a master regulator of FzD/G‐ protein signaling.

TL;DR: A novel way to assess WNT-FZD interaction by live cell imaging is introduced allowing further mapping of WNT and FZD interactions and challenging previous experimental limitations.