Stimuli signaling reward availability potentiate and control relapse for up to 300 days of abstinence following cocaine, but not food, self-administration in rats.

Hypothemycin, which inhibits a number of protein kinases, kills the T. brucei parasites that cause sleeping sickness and reveals new therapeutic targets for the disorder.

Cryo electron tomography provides the first high-resolution 3D axoneme structure from any pathogenic organism, revealing novel structures that support the unique motility of these pathogens through host tissues.

Single-cell transcriptomics of cryopreserved parasites reveals extensive cyclic regulation of mRNA abundance by Trypanosoma brucei during the cell cycle.

The ligand specificity and expression profile of the haptoglobin-haemoglobin receptor has diversified throughout the evolution of trypanosomes.

Global relative mRNA and protein abundance in trypanosomatids can be effectively estimated at transcriptomic and proteomic scales based on protein-coding sequences alone.

Toxic IAPP intermediates have some molecular features that are similar to, and others that are distinct from, toxic species reported for other amyloidogenic polypeptides.

A minimal subset of two to three residues in cyclic nucleotide binding (CNB) domains controls nucleoside vs. cyclic nucleotide specificity, repurposing PKA of certain pathogens for novel nucleoside signaling pathways or sensing.

Nuclear phosphoinositide signaling controls telomeric gene repression and activation essential for switching expression of surface antigen genes and thus antigenic variation.

The SPARC complex directs accurate RNAPII positioning for transcription initiation and, in some instances, ensures correct transcription directionality in Trypanosoma brucei.