<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14(6)</volume><submitter>Thomas M</submitter><pubmed_abstract>The human polycistronic miRNA cluster miR-17-92 is frequently overexpressed in hematopoietic malignancies and cancers. Its transcription is in part controlled by an E2F-regulated host gene promoter. An intronic A/T-rich region directly upstream of the miRNA coding region also contributes to cluster expression. Our deletion analysis of the A/T-rich region revealed a strong dependence on c-Myc binding to the functional E3 site. Yet, constructs lacking the 5'-proximal ~1.3 kb or 3'-distal ~0.1 kb of the 1.5 kb A/T-rich region still retained residual specific promoter activity, suggesting multiple transcription start sites (TSS) in this region. Furthermore, the protooncogenic kinase, Pim-1, its phosphorylation target HP1γ and c-Myc colocalize to the E3 region, as inferred from chromatin immuno</pubmed_abstract><journal>International journal of molecular sciences</journal><pagination>12273-96</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3709785</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Analysis of transcriptional regulation of the human miR-17-92 cluster; evidence for involvement of Pim-1.</pubmed_title><pmcid>PMC3709785</pmcid><pubmed_authors>Thomas M</pubmed_authors><pubmed_authors>Grunweller A</pubmed_authors><pubmed_authors>Golde L</pubmed_authors><pubmed_authors>Aigner A</pubmed_authors><pubmed_authors>Hartmann D</pubmed_authors><pubmed_authors>Lange-Grunweller K</pubmed_authors><pubmed_authors>Schlereth J</pubmed_authors><pubmed_authors>Streng D</pubmed_authors><pubmed_authors>Hartmann RK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Analysis of transcriptional regulation of the human miR-17-92 cluster; evidence for involvement of Pim-1.</name><description>The human polycistronic miRNA cluster miR-17-92 is frequently overexpressed in hematopoietic malignancies and cancers. Its transcription is in part controlled by an E2F-regulated host gene promoter. An intronic A/T-rich region directly upstream of the miRNA coding region also contributes to cluster expression. Our deletion analysis of the A/T-rich region revealed a strong dependence on c-Myc binding to the functional E3 site. Yet, constructs lacking the 5'-proximal ~1.3 kb or 3'-distal ~0.1 kb of the 1.5 kb A/T-rich region still retained residual specific promoter activity, suggesting multiple transcription start sites (TSS) in this region. Furthermore, the protooncogenic kinase, Pim-1, its phosphorylation target HP1γ and c-Myc colocalize to the E3 region, as inferred from chromatin immuno</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Jun</publication><modification>2026-04-08T17:03:31.495Z</modification><creation>2019-03-27T01:12:56Z</creation></dates><accession>S-EPMC3709785</accession><cross_references><pubmed>23749113</pubmed><doi>10.3390/ijms140612273</doi></cross_references></HashMap>