Plasmodium falciparum invasion protein EBA-175, once shed from the parasite surface post invasion, facilitates RBC clustering and enhances parasite growth while simultaneously enabling parasite immune evasion of host neutralizing antibodies.

The structure of the promising malaria blood-stage vaccine candidate antigen PfCyRPA and the characterization of a protective epitope are facilitating research on its essential role in parasite invasion, and will guide future epitope-focused vaccine design.

By moving from correlations to causality in cancer signal transduction using optogenetics, the sufficiency of RalB activation to trigger invasion and the underlying molecular mechanisms were established.

T antigen glycosylation, which marks metastatic cancer cells, is modulated on a small set of proteins by a conserved multipass transmembrane protein to allow tissue invasion by Drosophila macrophages.

An aspartyl protease is essential for the lytic cycle of Toxoplasma gondii and is involved in the maturation of proteins critical for invasion and egress, and it can be targeted selectively with an ethylamine scaffold based peptidomimetic inhibitor.

p27Kip1 directly controls invadopodia turnover by promoting the interaction of PAK1 with Cortactin, which induces Cortactin phosphorylation, invadopodia disassembly and facilitates invasion through extracellular matrix.

Gene knockdowns reveal that the conserved RhopH protein complex functions in both host cell invasion and channel-mediated nutrient uptake in malaria.

Interaction of P. falciparum with the erythrocyte activates a phosphorylation cascade altering the viscoelastic properties of this area of the host membrane conditioning it for successful invasion.

siRNA knockdown experiments reveal in detail the signaling pathway that controls cytoskeletal function during cell-in-cell invasion.

Clinical analysis corroborated with experimental data demonstrate that Δ133p53β, a naturally occurring isoform of p53 protein, induces a pro-metastatic program and is a clinical indicator of metastasis, independently of TP53 mutation status.