Jun. 4, 2020—Leslie Gewin and colleagues have upended conventional dogma about Wnt/beta-catenin signaling in the kidney, finding that it protects against chronic kidney disease rather than promoting it.
May. 19, 2020—Manuel Ascano team validates an inhibitor of the cGAS-STING signaling pathway, which is important for cellular innate immunity against bacteria, viruses, and our own damaged DNA.
May. 14, 2020—Vanderbilt researchers discover how anthrax bacterium defends itself against structural damage and resists the toxicity of the antimicrobial drug targocil.
May. 5, 2020—John York and colleagues have demonstrated that the protein Vip1 is a rare type of bifunctional enzyme: it can both synthesize and destroy key cellular signaling molecules.
Apr. 21, 2020—A disease-associated mutation in a transporter protein impairs gut barrier function, leading to gastrointestinal disease and chronic infections.
Apr. 20, 2020—Dylan Burnette and colleagues have discovered that two forms of the molecular motor protein myosin have distinct roles in regulating cell shape during cell division.
Apr. 20, 2020—New findings suggest that treatments that decrease oxidative damage might help with postoperative delirium that occurs in up to 30% of cardiac surgery patients.
Apr. 8, 2020—Danny Winder and colleagues are teasing apart the actions of neurotransmitter receptors in a brain region linked to anxiety and addiction, with a goal of finding treatments for substance use disorders.
Apr. 8, 2020—New insights on influenza genome packaging could guide strategies for interfering with the virus's life cycle and ability to cause infection.
Mar. 5, 2020—Jennifer Sucre and colleagues have discovered a factor that contributes to the pathological changes of bronchopulmonary dysplasia, the most common complication of preterm birth.
Feb. 25, 2020—The identification of novel protein interactions and sites of modification in proteins involved in mRNA translation adds to understanding of a process that is an important therapeutic target.
Feb. 20, 2020—A disease-associated mutation in a transporter protein causes cells to increase energy production, as if they are starving, Vanderbilt researchers have discovered.