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.
With monoubiquitination sites of Rab5 identified and structural and biochemical studies using chemically synthesized ubiquitinated Rab5, Rab5 monoubiquitination is found to downregulate the function of Rab5 in a site-dependent manner.
The human NimA-related kinases (Neks) recognize divergent substrate motifs, and include Nek10 as a dual-specificity serine/tyrosine kinase, and Nek6, Nek7 and Nek9 as amplifiers of the Plk1 phospho-motif.
A cell-surface receptor called Gpr52 is able to lower the levels of the disease-causing protein mutant huntingtin and suppress its toxicity when knocked-down, making this receptor a promising drug target in Huntington's disease.
Experiments in C. elegans reveal how synaptotagmin and Rab3, the 'yin and yang' of synapses, control whether transmitter vesicles remain docked at the presynaptic membrane or release their contents into the synapse.
A single point mutation in a Ras activator leads to aberrant constitutive mTOR signaling in peripheral T cells that consequently accumulate as abnormal T helper cells and stimulate the production of autoantibodies by B cells.
Neurexin–Neuroligin1 complex positively regulates F-actin assembly through direct interaction with WAVE complex to control normal synaptic growth and electrophysiological function in Drosophila neuromuscular junction.