By binding to Fc gamma receptor IIb, amyloid beta induces a series of phosphorylation events that mediate the damaging effects of hyperphosphorylated tau proteins in Alzheimer's disease.
A dual-color TIRFM study reveals a new form of inflammatory regulation, in which a lipid kinase and ion channel reciprocally regulate each other to amplify the response to painful stimuli.
Structural and biochemical data suggest a mechanism for the Synaptojanin1-catalysed reaction and the role of mutations in the onset of associated neurological diseases.
A novel innate defense mechanism of cell lysis involves the coordinated oligomerization of a defensin by interaction with the membrane lipid, phosphatidylinositol 4,5-bisphosphate.
The lipid kinase VPS34 complexes I and II are both activated by unsaturation of substrate and non-substrate lipids, curvature, electrostatics and polyphosphoinositides, which play roles in localisation and cellular function.
Ankyrin-B – through interactions with PI3P lipids, dynactin and RabGAP1L – functions as a critical node in the protein circuitry underlying polarized recycling of α5β1-integrin to enable haptotaxis along fibronectin gradients.