Modulation of dermal adipocytes contributes to skin homeostasis and provides a promising new therapeutic strategy in the treatment of EGFRI-related skin disorders.

Combined genetic experiments and cellular trafficking assays in Drosophila and mammalian models uncover a new role of RAS-like GTPases in EGFR signalling activation during tissue regeneration and tumourigenesis through regulation of EGFR internalisation.

Functional genomic screening reveals new synthetic lethality with and modes of resistance to epidermal growth factor receptor (EGFR) targeted therapy in EGFR-mutant human lung cancer.

The representations of information concerning the number, size, density and surface of sets of objects in a visual image are separable along the occipito-parietal cortex and independently modulated by attention.

Plasticity arising from autocatalytic receptor activation coexists with robustness in ligand responsiveness only by differential endosomal sorting of spontaneous and ligand-activated EGFR as distinct molecular states.

SOX2 causes resistance to anti-EGFR therapies in EGFR-mutant lung cancer.

The structural basis for Her2's role as a dedicated heterodimerization partner for other EGFR family receptors is elucidated with long-timescale atomistic simulations.

In the adult Drosophila testis, normally quiescent niche cells can be forced to re-enter the cell cycle and give rise to new stem cells in response to epidermal growth factor receptor signaling.

A small pool of active epidermal growth factor (EGF) receptors, which are capable of ubiquitylation and efficient endocytosis in vivo, is sufficient to support EGF-receptor-dependent tumor growth by signaling primarily through the Ras-MAPK pathway.

The local PI(4,5)P₂ nanodomain promotes the dimerization and activation of EGFR in the plasma membrane, whereas activated EGFR dissolves the nanodomain structure of PI(4,5)P₂ through PLCγ.