<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>15</volume><submitter>Hirschfeld M</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Estrogen receptor alpha (ERa/ESR1) expression is regulated by alternative splicing. Its most frequently detectable exon7 skipping isoform (ERaD7) is a dominant negative variant. Elevated expression of ERaD7 was already detected in endometrial cancer (EC), while its potential prognostic significance has not been characterized so far. Exon7 contains potential binding sites for the two functional splicing regulatory opponents, HNRNPG and HTRA2-BETA1 known to trigger opposite effects on EC outcome. This study served to elucidate the influence of HNRNPG and HTRA2-BETA1 on ERa exon7 splicing regulation and the impact of ERaD7 concentration on type 1 EC outcome.&lt;h4>Methods&lt;/h4>Functional in vitro experiments for HNRNPG and HTRA2-BETA1 in regard to the regulatory impact on endog</pubmed_abstract><journal>BMC cancer</journal><pagination>86</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4355463</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>HNRNP G and HTRA2-BETA1 regulate estrogen receptor alpha expression with potential impact on endometrial cancer.</pubmed_title><pmcid>PMC4355463</pmcid><pubmed_authors>Stickeler E</pubmed_authors><pubmed_authors>Orlowska-Volk M</pubmed_authors><pubmed_authors>Zur Hausen A</pubmed_authors><pubmed_authors>Jaeger M</pubmed_authors><pubmed_authors>Hirschfeld M</pubmed_authors><pubmed_authors>Ouyang YQ</pubmed_authors><pubmed_authors>Erbes T</pubmed_authors></additional><is_claimable>false</is_claimable><name>HNRNP G and HTRA2-BETA1 regulate estrogen receptor alpha expression with potential impact on endometrial cancer.</name><description>&lt;h4>Background&lt;/h4>Estrogen receptor alpha (ERa/ESR1) expression is regulated by alternative splicing. Its most frequently detectable exon7 skipping isoform (ERaD7) is a dominant negative variant. Elevated expression of ERaD7 was already detected in endometrial cancer (EC), while its potential prognostic significance has not been characterized so far. Exon7 contains potential binding sites for the two functional splicing regulatory opponents, HNRNPG and HTRA2-BETA1 known to trigger opposite effects on EC outcome. This study served to elucidate the influence of HNRNPG and HTRA2-BETA1 on ERa exon7 splicing regulation and the impact of ERaD7 concentration on type 1 EC outcome.&lt;h4>Methods&lt;/h4>Functional in vitro experiments for HNRNPG and HTRA2-BETA1 in regard to the regulatory impact on endog</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Feb</publication><modification>2026-06-10T08:52:28.154Z</modification><creation>2019-06-06T14:06:39Z</creation></dates><accession>S-EPMC4355463</accession><cross_references><pubmed>25884434</pubmed><doi>10.1186/s12885-015-1088-1</doi></cross_references></HashMap>