<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Scagnoli F</submitter><funding>by Minitero Università e Ricerca and CNR</funding><funding>Ministero Università e Ricerca and CNR</funding><funding>Italian Association for Cancer Research</funding><funding>AIRC IG</funding><pagination>412</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9952900</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(2)</volume><pubmed_abstract>MYC oncoprotein deregulation is a common catastrophic event in human cancer and limiting its activity restrains tumor development and maintenance, as clearly shown via Omomyc, an MYC-interfering 90 amino acid mini-protein. MYC is a multifunctional transcription factor that regulates many aspects of transcription by RNA polymerase II (RNAPII), such as transcription activation, pause release, and elongation. MYC directly associates with Protein Arginine Methyltransferase 5 (PRMT5), a protein that methylates a variety of targets, including RNAPII at the arginine residue R1810 (R1810me2s), crucial for proper transcription termination and splicing of transcripts. Therefore, we asked whether MYC controls termination as well, by affecting R1810me2S. We show that MYC overexpression strongly increa</pubmed_abstract><journal>Biomedicines</journal><pubmed_title>A New Insight into MYC Action: Control of RNA Polymerase II Methylation and Transcription Termination.</pubmed_title><pmcid>PMC9952900</pmcid><funding_grant_id>15927</funding_grant_id><funding_grant_id>Flagship Epigen Project</funding_grant_id><pubmed_authors>Scagnoli F</pubmed_authors><pubmed_authors>Illi B</pubmed_authors><pubmed_authors>Nasi S</pubmed_authors><pubmed_authors>Palma A</pubmed_authors><pubmed_authors>Favia A</pubmed_authors><pubmed_authors>Scuoppo C</pubmed_authors></additional><is_claimable>false</is_claimable><name>A New Insight into MYC Action: Control of RNA Polymerase II Methylation and Transcription Termination.</name><description>MYC oncoprotein deregulation is a common catastrophic event in human cancer and limiting its activity restrains tumor development and maintenance, as clearly shown via Omomyc, an MYC-interfering 90 amino acid mini-protein. MYC is a multifunctional transcription factor that regulates many aspects of transcription by RNA polymerase II (RNAPII), such as transcription activation, pause release, and elongation. MYC directly associates with Protein Arginine Methyltransferase 5 (PRMT5), a protein that methylates a variety of targets, including RNAPII at the arginine residue R1810 (R1810me2s), crucial for proper transcription termination and splicing of transcripts. Therefore, we asked whether MYC controls termination as well, by affecting R1810me2S. We show that MYC overexpression strongly increa</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-06-25T03:22:31.323Z</modification><creation>2025-05-29T19:43:07.888Z</creation></dates><accession>S-EPMC9952900</accession><cross_references><pubmed>36830948</pubmed><doi>10.3390/biomedicines11020412</doi></cross_references></HashMap>