Abstract |
Ubiquitin C-terminal Hydrolase L1 (UCH-L1) has oncogenic properties and is highly expressed during malignancies. We recently documented that Epstein-Barr virus ( EBV) infection induces uch-l1 expression. Here we show that Kaposi's Sarcoma-associated herpesvirus (KSHV) infection induced UCH-L1 expression, via cooperation of KSHV Latency-Associated Nuclear Antigen (LANA) and RBP-Jκ and activation of the uch-l1 promoter. UCH-L1 expression was also increased in Primary Effusion Lymphoma (PEL) cells co-infected with KSHV and EBV compared with PEL cells infected only with KSHV, suggesting EBV augments the effect of LANA on uch-l1. EBV latent membrane protein 1 (LMP1) is one of the few EBV products expressed in PEL cells. Results showed that LMP1 was sufficient to induce uch-l1 expression, and co-expression of LMP1 and LANA had an additive effect on uch-l1 expression. These results indicate that viral latency products of both human γ-herpesviruses contribute to uch-l1 expression, which may contribute to the progression of lymphoid malignancies.
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Authors | Gretchen L Bentz, Anjali Bheda-Malge, Ling Wang, Julia Shackelford, Blossom Damania, Joseph S Pagano |
Journal | Virology
(Virology)
Vol. 448
Pg. 293-302
(Jan 05 2014)
ISSN: 1096-0341 [Electronic] United States |
PMID | 24314660
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Copyright | © 2013 Published by Elsevier Inc. |
Chemical References |
- Antigens, Viral
- EBV-associated membrane antigen, Epstein-Barr virus
- Nuclear Proteins
- UCHL1 protein, human
- Viral Matrix Proteins
- latency-associated nuclear antigen
- Ubiquitin Thiolesterase
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Topics |
- Antigens, Viral
(genetics, metabolism)
- Cell Line, Transformed
- Cell Transformation, Viral
- Epstein-Barr Virus Infections
(enzymology, genetics, virology)
- Herpesviridae Infections
(enzymology, genetics, virology)
- Herpesvirus 4, Human
(genetics, metabolism)
- Herpesvirus 8, Human
(genetics, metabolism)
- Humans
- Nuclear Proteins
(genetics, metabolism)
- Ubiquitin Thiolesterase
(genetics, metabolism)
- Up-Regulation
- Viral Matrix Proteins
(genetics, metabolism)
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