Jost Enninga

Role of nucleoporin induction in releasing an mRNA nuclear export block.

Depletion of a single nucleoporin, Nup107, prevents the assembly of a subset of nucleoporins into the nuclear pore complex.

Sec13 shuttles between the nucleus and the cytoplasm and stably interacts with Nup96 at the nuclear pore complex.

VSV disrupts the Rae1/mrnp41 mRNA nuclear export pathway.

Tyrosine kinase signaling and type III effectors orchestrating Shigella invasion.

Secretion of type III effectors into host cells in real time.

Actin polymerisation at the cytoplasmic face of eukaryotic nuclei.

A course with a difference. Fighting infectious diseases with technology and knowledge-transfer.

Roundtrip explorations of bacterial infection: from single cells to the entire host and back.

Invasive and adherent bacterial pathogens co-Opt host clathrin for infection.

Turning on the spotlight--using light to monitor and characterize bacterial effector secretion and translocation.

The IpaC carboxyterminal effector domain mediates Src-dependent actin polymerization during Shigella invasion of epithelial cells.

Prions hijack tunnelling nanotubes for intercellular spread.

Imaging the assembly, structure and activity of type III secretion systems.

Galectin-3, a marker for vacuole lysis by invasive pathogens.

Tracking the dynamic interplay between bacterial and host factors during pathogen-induced vacuole rupture in real time.

The 'when and whereabouts' of injected pathogen effectors.

Tracking the secretion of fluorescently labeled type III effectors from single bacteria in real time.

Spotting the right location- imaging approaches to resolve the intracellular localization of invasive pathogens.

Monitoring Shigella flexneri vacuolar escape by flow cytometry.

Sec22b regulates phagosomal maturation and antigen crosspresentation by dendritic cells.

Phagosomal rupture by Mycobacterium tuberculosis results in toxicity and host cell death.

Hierarchies of host factor dynamics at the entry site of Shigella flexneri during host cell invasion.