David A. Pearce

TL;DR: A novel path of degeneration within the LGNd is defined, providing a mechanism for causation of JNCL visual deficits, and decreased transport of amino acids from the retina to the L GN is demonstrated, suggesting an impediment in communication between the retina and projection nuclei.

TL;DR: An overview of the therapeutic approaches currently being pursued in preclinical and clinical trials to treat different forms of NCL as well as insight to novel therapeutic approaches in development for the NCLs are provided.

TL;DR: It is demonstrated that Vpr functions as a GR coactivator and that this activity is independent of cell cycle arrest, and that the Vpr-induced coactivation requires an intact glucocorticoid response element and is mediated by the two highly conserved leucine-rich domains within Vpr that resemble the GR coActivator signature motif.

TL;DR: GILZ inhibition of ERK appears to play an essential role in stimulation of cell surface ENaC but not in inhibition of proliferation, and rat and mouse tissues all expressed multiple GILZ species but varied in the relative abundance of each.

TL;DR: It is strongly suggested that PC2-dependent processing of POMC into gamma-MSH is necessary for the normal response to the HSD, and a novel pathway mediating salt-sensitivity of blood pressure is demonstrated.