Andrew D. Yurochko

Human cytomegalovirus-caused damage to placental trophoblasts mediated by immediate-early gene-induced tumor necrosis factor-alpha.

DC-SIGN and L-SIGN can act as attachment receptors for alphaviruses and distinguish between mosquito cell- and mammalian cell-derived viruses.

Human cytomegalovirus induces monocyte differentiation and migration as a strategy for dissemination and persistence.

Activation of the NF-kappaB pathway in human cytomegalovirus-infected cells is necessary for efficient transactivation of the major immediate-early promoter.

HCMV activates PI(3)K in monocytes and promotes monocyte motility and transendothelial migration in a PI(3)K-dependent manner.

Human cytomegalovirus IE1-72 activates ataxia telangiectasia mutated kinase and a p53/p21-mediated growth arrest response.

Prolonged activation of NF-kappaB by human cytomegalovirus promotes efficient viral replication and late gene expression.

Human cytomegalovirus (HCMV) infection of endothelial cells promotes naive monocyte extravasation and transfer of productive virus to enhance hematogenous dissemination of HCMV.

The human cytomegalovirus virion possesses an activated casein kinase II that allows for the rapid phosphorylation of the inhibitor of NF-kappaB, IkappaBalpha.

Roles of phosphatidylinositol 3-kinase and NF-kappaB in human cytomegalovirus-mediated monocyte diapedesis and adhesion: strategy for viral persistence.

Transcriptome analysis of NF-kappaB- and phosphatidylinositol 3-kinase-regulated genes in human cytomegalovirus-infected monocytes.

Human CMV infection of endothelial cells induces an angiogenic response through viral binding to EGF receptor and beta1 and beta3 integrins.

Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.

NF-kappaB and phosphatidylinositol 3-kinase activity mediates the HCMV-induced atypical M1/M2 polarization of monocytes.

Activation of EGFR on monocytes is required for human cytomegalovirus entry and mediates cellular motility.

PI3K-dependent upregulation of Mcl-1 by human cytomegalovirus is mediated by epidermal growth factor receptor and inhibits apoptosis in short-lived monocytes.

Cytomegalovirus infection leads to microvascular dysfunction and exacerbates hypercholesterolemia-induced responses.

Human cytomegalovirus-regulated paxillin in monocytes links cellular pathogenic motility to the process of viral entry.

Human cytomegalovirus induction of a unique signalsome during viral entry into monocytes mediates distinct functional changes: a strategy for viral dissemination.

Human cytomegalovirus stimulates monocyte-to-macrophage differentiation via the temporal regulation of caspase 3.