Laura M. Bartle

TL;DR: Human cytomegalovirus (CMV), a herpesvirus that causes congenital disease and opportunistic infections in immunocompromised individuals, encodes functions that facilitate efficient viral propagation by altering host cell behavior and encodes a mitochondria-localized inhibitor of apoptosis, denoted vMIA, capable of suppressing apoptosis induced by diverse stimuli.

TL;DR: A human cytomegalovirus cell-death suppressor, denoted vICA, encoded by the viral UL36 gene is identified, which inhibits Fas-mediated apoptosis by binding to the pro-domain of caspase-8 and preventing its activation.

TL;DR: These results validate CD38 as a therapeutic target and support the current evaluation of this unique CD38-targeting functional antibody in phase I clinical trials in patients with CD38+ B-cell malignancies.

TL;DR: In vitro data suggest that NO, peroxynitrite, and HNE may directly act on ANT to induce mitochondrial membrane permeabilization and apoptosis.

TL;DR: It appears that vMIA is capable of suppressing apoptosis in cells in which this pathway is dominated by Bax, but not in cells where Bak also plays a role, and does not seem to either specifically associate with Bak or suppress Bak-mediated mitochondrial membrane permeabilization.