<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xu J</submitter><funding>Swiss National Science Foundation</funding><pagination>1344</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12897804</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(3)</volume><pubmed_abstract>The transcription factor &lt;i>DMP1&lt;/i> is a positive regulator of the tumor suppressor ARF, which in turn controls cell-cycle progression and/or apoptosis through p53. Given the role of DMP1 in the ARF-p53 pathway, we investigated whether the p53 transcription factor might regulate DMP1 expression. We found that endogenous human &lt;i>(h)DMP1&lt;/i> mRNA levels were significantly decreased upon induction of the temperature-sensitive p53&lt;sup>Val135&lt;/sup> in normal fibroblasts. Consistent with this observation, a p53 knockdown in MCF7 breast cancer cells resulted in increased &lt;i>hDMP1&lt;/i> mRNA and protein levels. At the molecular level, we found that p53 directly repressed the hDMP1 promoter activity by up to 90%. This repression was not mediated by p53 binding to the two putative p53-binding sites </pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Identification of DMP1 as Novel p53 Repressed Transcriptional Target.</pubmed_title><pmcid>PMC12897804</pmcid><funding_grant_id>173219</funding_grant_id><funding_grant_id>310030</funding_grant_id><funding_grant_id>31003A_173219</funding_grant_id><funding_grant_id>197786</funding_grant_id><funding_grant_id>310030_197786</funding_grant_id><pubmed_authors>Zlobec I</pubmed_authors><pubmed_authors>Torbett BE</pubmed_authors><pubmed_authors>Arvidsson G</pubmed_authors><pubmed_authors>Tschan MP</pubmed_authors><pubmed_authors>Britschgi C</pubmed_authors><pubmed_authors>Krauer D</pubmed_authors><pubmed_authors>Xu J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identification of DMP1 as Novel p53 Repressed Transcriptional Target.</name><description>The transcription factor &lt;i>DMP1&lt;/i> is a positive regulator of the tumor suppressor ARF, which in turn controls cell-cycle progression and/or apoptosis through p53. Given the role of DMP1 in the ARF-p53 pathway, we investigated whether the p53 transcription factor might regulate DMP1 expression. We found that endogenous human &lt;i>(h)DMP1&lt;/i> mRNA levels were significantly decreased upon induction of the temperature-sensitive p53&lt;sup>Val135&lt;/sup> in normal fibroblasts. Consistent with this observation, a p53 knockdown in MCF7 breast cancer cells resulted in increased &lt;i>hDMP1&lt;/i> mRNA and protein levels. At the molecular level, we found that p53 directly repressed the hDMP1 promoter activity by up to 90%. This repression was not mediated by p53 binding to the two putative p53-binding sites </description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-07-08T03:12:39.446Z</modification><creation>2026-07-08T03:08:30.384Z</creation></dates><accession>S-EPMC12897804</accession><cross_references><pubmed>41683766</pubmed><doi>10.3390/ijms27031344</doi></cross_references></HashMap>