<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Falquet M</submitter><funding>The Research Council of Norway</funding><funding>Northern Norway Regional Health Authority</funding><pagination>895</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9820997</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(1)</volume><pubmed_abstract>Merkel cell polyomavirus (MCPyV) is the major cause of Merkel cell carcinoma (MCC), an aggressive skin cancer. MCPyV large T-antigen (LTag) and small T-antigen (sTag) are the main oncoproteins involved in MCPyV-induced MCC. A hallmark of MCPyV-positive MCC cells is the expression of a C-terminal truncated LTag. Protein kinase A (PKA) plays a fundamental role in a variety of biological processes, including transcription by phosphorylating and thereby regulating the activity of transcription factors. As MCPyV LTag has been shown to be phosphorylated and acts as a transcription factor for the viral early and late promoter, we investigated whether LTag can be phosphorylayted by PKA, and whether this affects the transcript activity of LTag. Using a phosphorylation prediction algorithm, serine 1</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Regulation of Transcriptional Activity of Merkel Cell Polyomavirus Large T-Antigen by PKA-Mediated Phosphorylation.</pubmed_title><pmcid>PMC9820997</pmcid><funding_grant_id>295910</funding_grant_id><funding_grant_id>HNF1441-18 and HNF1596-21</funding_grant_id><pubmed_authors>Passerini S</pubmed_authors><pubmed_authors>Ludvigsen M</pubmed_authors><pubmed_authors>Moens U</pubmed_authors><pubmed_authors>Prezioso C</pubmed_authors><pubmed_authors>Sveinbjornsson B</pubmed_authors><pubmed_authors>Bruun JA</pubmed_authors><pubmed_authors>Pietropaolo V</pubmed_authors><pubmed_authors>Falquet M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of Transcriptional Activity of Merkel Cell Polyomavirus Large T-Antigen by PKA-Mediated Phosphorylation.</name><description>Merkel cell polyomavirus (MCPyV) is the major cause of Merkel cell carcinoma (MCC), an aggressive skin cancer. MCPyV large T-antigen (LTag) and small T-antigen (sTag) are the main oncoproteins involved in MCPyV-induced MCC. A hallmark of MCPyV-positive MCC cells is the expression of a C-terminal truncated LTag. Protein kinase A (PKA) plays a fundamental role in a variety of biological processes, including transcription by phosphorylating and thereby regulating the activity of transcription factors. As MCPyV LTag has been shown to be phosphorylated and acts as a transcription factor for the viral early and late promoter, we investigated whether LTag can be phosphorylayted by PKA, and whether this affects the transcript activity of LTag. Using a phosphorylation prediction algorithm, serine 1</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-21T16:21:23.832Z</modification><creation>2025-04-21T16:21:23.832Z</creation></dates><accession>S-EPMC9820997</accession><cross_references><pubmed>36614338</pubmed><doi>10.3390/ijms24010895</doi></cross_references></HashMap>