Publications by authors named "H P Barth"

Embedding of cell-surface receptors into a membrane defines their dynamics but also complicates experimental characterization of their signaling complexes. The hepatocyte growth factor receptor MET is a receptor tyrosine kinase involved in cellular processes such as proliferation, migration, and survival. It is also targeted by the pathogen Listeria monocytogenes, whose invasion protein, internalin B (InlB), binds to MET, forming a signaling dimer that triggers pathogen internalization.

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Pertussis (whooping cough) is a vaccine-preventable but re-emerging, highly infectious respiratory disease caused by Bordetella pertussis. There are currently no effective treatments for pertussis, complicating care for nonvaccinated individuals, especially newborns. Disease manifestations are predominantly caused by pertussis toxin (PT), a pivotal virulence factor classified as an ADP-ribosylating AB-type protein toxin.

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Article Synopsis
  • Many bacteria release AB-type protein toxins that disrupt cell functions, causing illness; targeting these toxins could lead to new treatments.
  • The FDA-approved drug disulfiram (DSF), typically used for alcohol dependence, shows potential in protecting cells from various toxins at low concentrations.
  • DSF appears to inhibit the translocation of toxic A subunits into cells without significantly affecting toxin binding or activity.
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Autophagy is an evolutionarily ancient catabolic pathway and has recently emerged as an integral part of the innate immune system. While the core machinery of autophagy is well defined, the physiological regulation of autophagy is less understood. Here, we identify a C-terminal fragment of human hemoglobin A (HBA1, amino acids 111-132) in human bone marrow as a fast-acting non-inflammatory inhibitor of autophagy initiation.

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Article Synopsis
  • The bacterium Clostridium botulinum produces C2 toxin, which is a binary AB-toxin that disrupts the cytoskeleton of cells, leading to cell death.
  • C2 toxin consists of an active A-component (C2I) and a binding B-component (C2II), which together enter cells and mediate their toxic effects by ADP-ribosylating G-actin.
  • The serine-protease inhibitor α-antitrypsin (αAT) can inhibit the effects of C2 toxin and other toxins, suggesting its potential repurposing as a treatment for diseases caused by these toxins.
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