<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sun Y</submitter><funding>NCI NIH HHS</funding><pagination>1794-810</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3427418</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>32(14)</volume><pubmed_abstract>The RPS6KA6 gene encodes the p90 ribosomal S6 kinase-4 (RSK4) that is still largely uncharacterized. In this study we identified a new RSK4 transcription initiation site and several alternative splice sites with a 5'-RACE approach. The resulting mRNA variants encompass four possible first start codons. The first 15 nucleotides (nt) of exon 22 in mouse and the penultimate exon in both human (exon 21) and mouse (exon 24) RSK4 underwent alternative splicing, although the penultimate exon deleted variant appeared mainly in cell clines, but not in most normal tissues. Demethylation agent 5-azacytidine inhibited the deletion of the penultimate exon, whereas two indolocarbazole-derived inhibitors of cyclin-dependent kinase 4 or 6 induced deletion of the first 39 nt from exon 21 of human RSK4. In </pubmed_abstract><journal>Oncogene</journal><pubmed_title>Basic anatomy and tumor biology of the RPS6KA6 gene that encodes the p90 ribosomal S6 kinase-4.</pubmed_title><pmcid>PMC3427418</pmcid><funding_grant_id>R01 CA100864</funding_grant_id><pubmed_authors>Yang M</pubmed_authors><pubmed_authors>Wu S</pubmed_authors><pubmed_authors>Cao S</pubmed_authors><pubmed_authors>Lin X</pubmed_authors><pubmed_authors>Liao DJ</pubmed_authors><pubmed_authors>Song X</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Basic anatomy and tumor biology of the RPS6KA6 gene that encodes the p90 ribosomal S6 kinase-4.</name><description>The RPS6KA6 gene encodes the p90 ribosomal S6 kinase-4 (RSK4) that is still largely uncharacterized. In this study we identified a new RSK4 transcription initiation site and several alternative splice sites with a 5'-RACE approach. The resulting mRNA variants encompass four possible first start codons. The first 15 nucleotides (nt) of exon 22 in mouse and the penultimate exon in both human (exon 21) and mouse (exon 24) RSK4 underwent alternative splicing, although the penultimate exon deleted variant appeared mainly in cell clines, but not in most normal tissues. Demethylation agent 5-azacytidine inhibited the deletion of the penultimate exon, whereas two indolocarbazole-derived inhibitors of cyclin-dependent kinase 4 or 6 induced deletion of the first 39 nt from exon 21 of human RSK4. In </description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Apr</publication><modification>2026-04-29T10:47:34.296Z</modification><creation>2019-03-27T00:57:10Z</creation></dates><accession>S-EPMC3427418</accession><cross_references><pubmed>22614021</pubmed><doi>10.1038/onc.2012.200</doi></cross_references></HashMap>