Clare E. Sample
Penn State Cancer Institute
42 Papers
779 Citations
Clare E. Sample is an academic researcher from Penn State Cancer Institute. The author has contributed to research in topics: Epstein–Barr virus & Virus. The author has an hindex of 23, co-authored 39 publications. Previous affiliations of Clare E. Sample include University of Tennessee & St. Jude Children's Research Hospital.
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Papers
Subnuclear localization and phosphorylation of Epstein-Barr virus latent infection nuclear proteins.
TL;DR: Using antibodies specific for each EBNA in immunofluorescence microscopy,EBNA-2, -3A, and -3C localized to subnuclear granules which fill much of the nucleus, excluding nucleoli, while EBNA-LP localized to a small number of discrete subnuclear particles, also excludingucleoli.
146
Epstein-Barr virus nuclear antigen 3C is a transcriptional regulator.
Dana Marshall,Clare E. Sample +1 more
TL;DR: Using transient transfection assays, it is demonstrated that EBNA-3C has two effects on reporter genes that are linked to the latent membrane protein 1 promoter, low-level activation by EBNA -3C alone, as well as potentiation ofEBNA-2-mediated transactivation, and inhibition of the normally strong activation mediated by EB NA-2.
130
Efficient replication of Epstein-Barr virus in stratified epithelium in vitro.
Rachel M. Temple,Junjia Zhu,Lynn R. Budgeon,Neil D. Christensen,Craig Meyers,Clare E. Sample +5 more
TL;DR: It is demonstrated that EBV is able to infect organotypic cultures of epithelial cells to establish a predominantly productive infection in the suprabasal layers of stratified epithelium, similar to that seen with Kaposi’s-associated herpesvirus.
129
A conserved domain of the Epstein-Barr virus nuclear antigens 3A and 3C binds to a discrete domain of Jkappa.
TL;DR: The ability of the EBNA-3 proteins to prevent Jkappa from binding to DNA in vitro and suppress transactivation via Jkappas DNA elements suggests that theEBNA- 3 proteins act analogously to the Drosophila protein Hairless.
123
Epstein-Barr Virus DNA Recombination and Loss in Sporadic Burkitt's Lymphoma
TL;DR: Identification of defective, integrated viral DNA in some tumors indicates greater involvement of virus in sporadic Burkitt's lymphoma than previously documented and suggests a process of viral DNA rearrangement and loss during malignant progression most consistent with an initiating role for EBV in tumorigenesis.