Excitotoxicity mediated by the N-methyl-D-aspartate receptor (NMDAR) is believed to be a primary mechanism of neuronal injury following stroke.Thus, many drugs and therapeutic peptides were developed to inhibit either the NMDAR at the cell surface or its downstream intracellular death-signaling cascades.Nevertheless, the majority of focal ischemia
Elias Oussedik,1 Capri G Foy,2 E J Masicampo,3 Lara K Kammrath,3 Robert E Anderson,1 Steven R Feldman1,4,5 1Center for Dermatology Research, Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, NC, USA; 2Department of Social Sciences and Health Policy, Wake Washer Dryer Forest School of Medicine, Winston-Salem, NC, USA; 3Depart
Gaseous carbon dioxide enters the biosphere almost exclusively via the active site of the enzyme ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco).This highly conserved catalyst has an almost universal propensity to non-productively interact with its substrate ribulose 1,5-bisphosphate, leading to the formation of dead-end inhibited complex