<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Larsson O</submitter><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>4375-86</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1636353</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>34(16)</volume><pubmed_abstract>Aberrant activation of the translation initiation machinery is a common property of malignant cells, and is essential for breast carcinoma cells to manifest a malignant phenotype. How does sustained activation of the rate limiting step in protein synthesis so fundamentally alter a cell? In this report, we test the post transcriptional operon theory as a possible mechanism, employing a model system in which apoptosis resistance is conferred on NIH 3T3 cells by ectopic expression of eIF4E. We show (i) there is a set of 255 transcripts that manifest an increase in translational efficiency during eIF4E-mediated escape from apoptosis; (ii) there is a novel prototype 55 nt RNA consensus hairpin structure that is overrepresented in the 5'-untranslated region of translationally activated transcrip</pubmed_abstract><journal>Nucleic acids research</journal><pubmed_title>Apoptosis resistance downstream of eIF4E: posttranscriptional activation of an anti-apoptotic transcript carrying a consensus hairpin structure.</pubmed_title><pmcid>PMC1636353</pmcid><funding_grant_id>HL073719</funding_grant_id><funding_grant_id>T32 HL07741</funding_grant_id><funding_grant_id>P50 HL50152</funding_grant_id><funding_grant_id>K08 HL074058</funding_grant_id><funding_grant_id>P01 AI050162</funding_grant_id><funding_grant_id>R01 HL076779</funding_grant_id><funding_grant_id>HL076779</funding_grant_id><funding_grant_id>T32 HL007741</funding_grant_id><funding_grant_id>1K08-HL074058-01</funding_grant_id><funding_grant_id>R01 HL073719</funding_grant_id><funding_grant_id>P01 AI50162</funding_grant_id><pubmed_authors>Polunovsky VA</pubmed_authors><pubmed_authors>Peterson M</pubmed_authors><pubmed_authors>Larsson O</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Bitterman PB</pubmed_authors><pubmed_authors>Liang Z</pubmed_authors><pubmed_authors>Reilly CS</pubmed_authors><pubmed_authors>Dahlgren C</pubmed_authors><pubmed_authors>Perlman DM</pubmed_authors><pubmed_authors>Fan D</pubmed_authors><pubmed_authors>Wahlestedt C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Apoptosis resistance downstream of eIF4E: posttranscriptional activation of an anti-apoptotic transcript carrying a consensus hairpin structure.</name><description>Aberrant activation of the translation initiation machinery is a common property of malignant cells, and is essential for breast carcinoma cells to manifest a malignant phenotype. How does sustained activation of the rate limiting step in protein synthesis so fundamentally alter a cell? In this report, we test the post transcriptional operon theory as a possible mechanism, employing a model system in which apoptosis resistance is conferred on NIH 3T3 cells by ectopic expression of eIF4E. We show (i) there is a set of 255 transcripts that manifest an increase in translational efficiency during eIF4E-mediated escape from apoptosis; (ii) there is a novel prototype 55 nt RNA consensus hairpin structure that is overrepresented in the 5'-untranslated region of translationally activated transcrip</description><dates><release>2006-01-01T00:00:00Z</release><publication>2006</publication><modification>2026-05-02T19:44:40.792Z</modification><creation>2019-03-27T01:46:14Z</creation></dates><accession>S-EPMC1636353</accession><cross_references><pubmed>16936314</pubmed><doi>10.1093/nar/gkl558</doi></cross_references></HashMap>