Macropinocytosis, the process of non-specific endocytosis, is a major gateway for large volumes of surrounding medium and nanoparticles to coral cells.

Inactivation of the Dictyostelium orthologue of the tumour suppressor Neurofibromin (NF1) enables amoebae to ingest dissolved nutrients using macropinocytosis more rapidly, and to prey on larger organisms using phagocytosis.

The archetypal tumor promoter PMA, which promotes cancer without mutating the DNA, increases Wnt signaling by activating macropinocytosis and membrane trafficking in Xenopus embryos and tumor cells.

Exosomes from cancer-associated fibroblasts enhance the "Warburg effect" in tumors and contain de novo metabolites that can contribute to the entire compendia of central carbon metabolism within cancer cells.

Rings of actin polymerisation that form around PIP3/Ras patches in the cell membrane drive the formation of macropinocytic cups.

Inhibition of GOT2 drives growth inhibitory reductive stress that can be rescued by electron acceptors in vitro, whereas GOT2 inhibition in endogenous or transplanted tumor models is tolerated without consequence, highlighting the importance of context when studying tumor metabolism.

Pancreatic cancers can utilize hyaluronic acid, an abundant extracellular matrix component in the tumor microenvironment, to fuel cancer cell metabolism and growth.

The cellular behaviours that underlie the internalization of the multilayered endoderm anlage in Xenopus laevis link the ancestral mode of vertebrate gastrulation to common, epithelial-based mechanisms of gastrulation in non-vertebrate animals.

Co-mutation of two powerful oncogenes in certain cell types may have a lethal effect that explains the mutual exclusivity of the mutations.

Activation by amino acids causes mTORC1 to translocate transiently to the lysosomal surface.