<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Abad E</submitter><funding>Agencia Estatal de Investigación</funding><funding>Ministerio de Ciencia e Innovación</funding><funding>'la Caixa' Foundation</funding><funding>Fundación Científica Asociación Española Contra el Cáncer</funding><funding>&amp;apos;la Caixa&amp;apos; Foundation</funding><pagination>127</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11057071</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>TP53, the most frequently mutated gene in human cancers, orchestrates a complex transcriptional program crucial for cancer prevention. While certain TP53-dependent genes have been extensively studied, others, like the recently identified RNF144B, remained poorly understood. This E3 ubiquitin ligase has shown potent tumor suppressor activity in murine Eμ Myc-driven lymphoma, emphasizing its significance in the TP53 network. However, little is known about its targets and its role in cancer development, requiring further exploration. In this work, we investigate RNF144B's impact on tumor suppression beyond the hematopoietic compartment in human cancers.&lt;h4>Methods&lt;/h4>Employing TP53 wild-type cells, we generated models lacking RNF144B in both non-transformed and cancerous c</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.</pubmed_title><pmcid>PMC11057071</pmcid><funding_grant_id>CEX2018-000792-M</funding_grant_id><funding_grant_id>51110009</funding_grant_id><funding_grant_id>POSTD234858ZADR</funding_grant_id><funding_grant_id>RYC2018-025244-I</funding_grant_id><funding_grant_id>PID2021-127710OB-I00</funding_grant_id><pubmed_authors>Romero G</pubmed_authors><pubmed_authors>Martinez CM</pubmed_authors><pubmed_authors>Janic A</pubmed_authors><pubmed_authors>Sandoz J</pubmed_authors><pubmed_authors>Weghorn D</pubmed_authors><pubmed_authors>Abad E</pubmed_authors><pubmed_authors>Kourtis S</pubmed_authors><pubmed_authors>Zadra I</pubmed_authors><pubmed_authors>Ortet L</pubmed_authors><pubmed_authors>Sdelci S</pubmed_authors><pubmed_authors>Urgel-Solas J</pubmed_authors><pubmed_authors>Borredat P</pubmed_authors></additional><is_claimable>false</is_claimable><name>The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.</name><description>&lt;h4>Background&lt;/h4>TP53, the most frequently mutated gene in human cancers, orchestrates a complex transcriptional program crucial for cancer prevention. While certain TP53-dependent genes have been extensively studied, others, like the recently identified RNF144B, remained poorly understood. This E3 ubiquitin ligase has shown potent tumor suppressor activity in murine Eμ Myc-driven lymphoma, emphasizing its significance in the TP53 network. However, little is known about its targets and its role in cancer development, requiring further exploration. In this work, we investigate RNF144B's impact on tumor suppression beyond the hematopoietic compartment in human cancers.&lt;h4>Methods&lt;/h4>Employing TP53 wild-type cells, we generated models lacking RNF144B in both non-transformed and cancerous c</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-05-29T12:36:29.856Z</modification><creation>2026-04-08T04:50:58.897Z</creation></dates><accession>S-EPMC11057071</accession><cross_references><pubmed>38685100</pubmed><doi>10.1186/s13046-024-03045-4</doi></cross_references></HashMap>