Ashlee V. Moses

Kaposi's sarcoma-associated herpesvirus-induced upregulation of the c-kit proto-oncogene, as identified by gene expression profiling, is essential for the transformation of endothelial cells.

A functional genomics approach to Kaposi's sarcoma.

Kaposi sarcoma-associated herpesvirus (KSHV) induces heme oxygenase-1 expression and activity in KSHV-infected endothelial cells.

Human immunodeficiency virus (HIV) type 1 Vpu induces the expression of CD40 in endothelial cells and regulates HIV-induced adhesion of B-lymphoma cells.

Increased efficiency of phorbol ester-induced lytic reactivation of Kaposi's sarcoma-associated herpesvirus during S phase.

Novel cellular genes essential for transformation of endothelial cells by Kaposi's sarcoma-associated herpesvirus.

Functional genomics and the development of pathogenesis-targeted therapies for Kaposi's sarcoma.

Kaposi sarcoma herpesvirus K5 removes CD31/PECAM from endothelial cells.

Insulin-like growth factor II receptor-mediated intracellular retention of cathepsin B is essential for transformation of endothelial cells by Kaposi's sarcoma-associated herpesvirus.

Human cytomegalovirus secretome contains factors that induce angiogenesis and wound healing.

Pathology of rituximab-induced Kaposi sarcoma flare.

Remodeling of endothelial adherens junctions by Kaposi's sarcoma-associated herpesvirus.

Characterization of c-Kit expression and activation in KSHV-infected endothelial cells.

Vpu directs the degradation of the human immunodeficiency virus restriction factor BST-2/Tetherin via a {beta}TrCP-dependent mechanism.

The inflammatory component of Kaposi sarcoma.

Molecular mechanism of BST2/tetherin downregulation by K5/MIR2 of Kaposi's sarcoma-associated herpesvirus.

The great escape: viral strategies to counter BST-2/tetherin.

Kaposi's sarcoma and human dermal microvascular endothelial cells infected with Kaposi's sarcoma-associated herpesvirus express CCL21.

Viral takeover of the host ubiquitin system.

Ubiquitination of BST-2 protein by HIV-1 Vpu protein does not require lysine, serine, or threonine residues within the BST-2 cytoplasmic domain.

Kaposi Sarcoma Pathogenesis: A Triad of Viral Infection, Oncogenesis and Chronic Inflammation.

CD31 immunohistochemical staining in Kaposi Sarcoma.

IRF-3, IRF-5, and IRF-7 coordinately regulate the type I IFN response in myeloid dendritic cells downstream of MAVS signaling.

A comparative mutational analysis of HIV-1 Vpu subtypes B and C for the identification of determinants required to counteract BST-2/Tetherin and enhance viral egress.

Aberrant proliferation in CXCR7+ endothelial cells via degradation of the retinoblastoma protein.

Comparative study of four immortalized human brain capillary endothelial cell lines, hCMEC/D3, hBMEC, TY10, and BB19, and optimization of culture conditions, for an in vitro blood-brain barrier model for drug permeability studies.

CXCR7 expression disrupts endothelial cell homeostasis and causes ligand-dependent invasion.

Ebola Virus Glycoprotein Promotes Enhanced Viral Egress by Preventing Ebola VP40 From Associating With the Host Restriction Factor BST2/Tetherin.

Kaposi Sarcoma Herpesvirus Induces HO-1 during De Novo Infection of Endothelial Cells via Viral miRNA-Dependent and -Independent Mechanisms.

The Heme Metabolite Carbon Monoxide Facilitates KSHV Infection by Inhibiting TLR4 Signaling in Endothelial Cells.