Alexandra Schubert-Unkmeir

Fibronectin mediates Opc-dependent internalization of Neisseria meningitidis in human brain microvascular endothelial cells.

Gene expression pattern in human brain endothelial cells in response to Neisseria meningitidis.

Expression of the meningococcal adhesin NadA is controlled by a transcriptional regulator of the MarR family.

Mammalian cell transcriptome in response to meningitis-causing pathogens.

Entry of Neisseria meningitidis into mammalian cells requires the Src family protein tyrosine kinases.

The transcriptional repressor FarR is not involved in meningococcal fatty acid resistance mediated by the FarAB efflux pump and dependent on lipopolysaccharide structure.

Neisseria meningitidis induces brain microvascular endothelial cell detachment from the matrix and cleavage of occludin: a role for MMP-8.

Characterization of FarR as a highly specialized, growth phase-dependent transcriptional regulator in Neisseria meningitidis.

Cell invasion by Neisseria meningitidis requires a functional interplay between the focal adhesion kinase, Src and cortactin.

Genome-based bacterial vaccines: current state and future outlook.

Role of epidermal growth factor receptor signaling in the interaction of Neisseria meningitidis with endothelial cells.

Disease and Carrier Isolates of Neisseria meningitidis Cause G1 Cell Cycle Arrest in Human Epithelial Cells.

Antibacterial activity of ceramide and ceramide analogs against pathogenic Neisseria.

Complement C5a Receptor 1 Exacerbates the Pathophysiology of Sepsis and Is a Potential Target for Disease Treatment.

The role of acid sphingomyelinase and modulation of sphingolipid metabolism in bacterial infection.

Differential influences of complement on neutrophil responses to Neisseria meningitidis infection.

In Vitro Models for Studying the Interaction of Neisseria meningitidis with Human Brain Endothelial Cells.

Neisseria meningitidis Type IV Pili Trigger Ca-Dependent Lysosomal Trafficking of the Acid Sphingomyelinase To Enhance Surface Ceramide Levels.

Induced Pluripotent Stem Cell-Derived Brain Endothelial Cells as a Cellular Model to Study Infection.

Streptococcus agalactiae disrupts P-glycoprotein function in brain endothelial cells.