File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1097/QAI.0b013e31817fbdcf
- Scopus: eid_2-s2.0-50949118028
- PMID: 18645521
- WOS: WOS:000258082200003
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Regulation of kaposi's sarcoma-associated herpesvirus reactivation by dopamine receptor-mediated signaling pathways
Title | Regulation of kaposi's sarcoma-associated herpesvirus reactivation by dopamine receptor-mediated signaling pathways |
---|---|
Authors | |
Keywords | Signal transduction Herpesvirus reactivation Dopamine KSHV |
Issue Date | 2008 |
Citation | Journal of Acquired Immune Deficiency Syndromes, 2008, v. 48, n. 5, p. 531-540 How to Cite? |
Abstract | BACKGROUND:: Kaposi's sarcoma-associated herpesvirus (KSHV) possesses two distinct life cycles, lytic replication and latency. An immediate early viral protein, Replication and transcription activator (RTA), is responsible for the virus switch from latency to active replication. METHODS:: To identify cellular pathways that reactivate KSHV replication, an RTA-responsive viral early promoter, PAN, coupled with an enhanced green fluorescent protein (EGFP) reporter was delivered into a KSHV latently infected B cell line. Five different chemical libraries with defined cellular targets were screened for their ability to induce the PAN promoter as an indication of lytic replication. RESULTS:: We identified seven chemicals that disrupted latency in KSHV latently infected B cells, five being N-acyl-dopamine derivatives. We showed that these chemicals reactivate KSHV through interacting with dopamine receptors, and that KSHV utilizes dopamine receptors and the associated PKA and MAP kinase pathways to detect and transmit stress signals for reactivation. CONCLUSION:: Our study identified two cellular signaling pathways that mediate KSHV reactivation and provided a chemical genetics approach to identify new endogenous activators with therapeutic potential against herpesvirus associated malignancies. © 2008 by Lippincott Williams & Wilkins. |
Persistent Identifier | http://hdl.handle.net/10722/285632 |
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 1.225 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Shaoying | - |
dc.contributor.author | Deng, Hongyu | - |
dc.contributor.author | Yu, Fuqu | - |
dc.contributor.author | Melega, William P. | - |
dc.contributor.author | Damoiseaux, Robert | - |
dc.contributor.author | Bradley, Kenneth A. | - |
dc.contributor.author | Sun, Ren | - |
dc.date.accessioned | 2020-08-18T04:56:15Z | - |
dc.date.available | 2020-08-18T04:56:15Z | - |
dc.date.issued | 2008 | - |
dc.identifier.citation | Journal of Acquired Immune Deficiency Syndromes, 2008, v. 48, n. 5, p. 531-540 | - |
dc.identifier.issn | 1525-4135 | - |
dc.identifier.uri | http://hdl.handle.net/10722/285632 | - |
dc.description.abstract | BACKGROUND:: Kaposi's sarcoma-associated herpesvirus (KSHV) possesses two distinct life cycles, lytic replication and latency. An immediate early viral protein, Replication and transcription activator (RTA), is responsible for the virus switch from latency to active replication. METHODS:: To identify cellular pathways that reactivate KSHV replication, an RTA-responsive viral early promoter, PAN, coupled with an enhanced green fluorescent protein (EGFP) reporter was delivered into a KSHV latently infected B cell line. Five different chemical libraries with defined cellular targets were screened for their ability to induce the PAN promoter as an indication of lytic replication. RESULTS:: We identified seven chemicals that disrupted latency in KSHV latently infected B cells, five being N-acyl-dopamine derivatives. We showed that these chemicals reactivate KSHV through interacting with dopamine receptors, and that KSHV utilizes dopamine receptors and the associated PKA and MAP kinase pathways to detect and transmit stress signals for reactivation. CONCLUSION:: Our study identified two cellular signaling pathways that mediate KSHV reactivation and provided a chemical genetics approach to identify new endogenous activators with therapeutic potential against herpesvirus associated malignancies. © 2008 by Lippincott Williams & Wilkins. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Acquired Immune Deficiency Syndromes | - |
dc.subject | Signal transduction | - |
dc.subject | Herpesvirus reactivation | - |
dc.subject | Dopamine | - |
dc.subject | KSHV | - |
dc.title | Regulation of kaposi's sarcoma-associated herpesvirus reactivation by dopamine receptor-mediated signaling pathways | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1097/QAI.0b013e31817fbdcf | - |
dc.identifier.pmid | 18645521 | - |
dc.identifier.scopus | eid_2-s2.0-50949118028 | - |
dc.identifier.volume | 48 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 531 | - |
dc.identifier.epage | 540 | - |
dc.identifier.isi | WOS:000258082200003 | - |
dc.identifier.issnl | 1525-4135 | - |