<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lieschke E</submitter><funding>DHAC | National Health and Medical Research Council</funding><funding>Harry Secomb Foundation</funding><funding>Victorian Cancer Agency</funding><funding>Dyson Bequest</funding><funding>The estate of Anthony Redstone OAM</funding><funding>Victorian Cancer Agency (VCA)</funding><funding>DHAC | National Health and Medical Research Council (NHMRC)</funding><funding>The Craig Perkins Cancer Research Foundation</funding><pagination>4406-4436</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11445477</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(19)</volume><pubmed_abstract>Investigating how transcription factors control complex cellular processes requires tools that enable responses to be visualised at the single-cell level and their cell fate to be followed over time. For example, the tumour suppressor p53 (also called TP53 in humans and TRP53 in mice) can initiate diverse cellular responses by transcriptional activation of its target genes: Puma to induce apoptotic cell death and p21 to induce cell cycle arrest/cell senescence. However, it is not known how these processes are regulated and initiated in different cell types. Also, the context-dependent interaction partners and binding loci of p53 remain largely elusive. To be able to examine these questions, we here developed knock-in mice expressing triple-FLAG-tagged p53 to facilitate p53 pull-down and tw</pubmed_abstract><journal>The EMBO journal</journal><pubmed_title>Mouse models to investigate in situ cell fate decisions induced by p53.</pubmed_title><pmcid>PMC11445477</pmcid><funding_grant_id>2011139</funding_grant_id><funding_grant_id>2002618</funding_grant_id><funding_grant_id>1154970</funding_grant_id><funding_grant_id>1116937</funding_grant_id><funding_grant_id>1143105</funding_grant_id><funding_grant_id>1113133</funding_grant_id><funding_grant_id>2010275</funding_grant_id><funding_grant_id>17028</funding_grant_id><funding_grant_id>2001201</funding_grant_id><pubmed_authors>Smyth GK</pubmed_authors><pubmed_authors>Kelly GL</pubmed_authors><pubmed_authors>Tai L</pubmed_authors><pubmed_authors>Atkin-Smith GK</pubmed_authors><pubmed_authors>Strasser A</pubmed_authors><pubmed_authors>Herold MJ</pubmed_authors><pubmed_authors>Thomas AF</pubmed_authors><pubmed_authors>La Marca JE</pubmed_authors><pubmed_authors>Lieschke E</pubmed_authors><pubmed_authors>Hawkins ED</pubmed_authors><pubmed_authors>Young S</pubmed_authors><pubmed_authors>Huang AS</pubmed_authors><pubmed_authors>Kueh A</pubmed_authors><pubmed_authors>Whelan L</pubmed_authors><pubmed_authors>Kaloni D</pubmed_authors><pubmed_authors>Baldoni PL</pubmed_authors><pubmed_authors>Ross AM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mouse models to investigate in situ cell fate decisions induced by p53.</name><description>Investigating how transcription factors control complex cellular processes requires tools that enable responses to be visualised at the single-cell level and their cell fate to be followed over time. For example, the tumour suppressor p53 (also called TP53 in humans and TRP53 in mice) can initiate diverse cellular responses by transcriptional activation of its target genes: Puma to induce apoptotic cell death and p21 to induce cell cycle arrest/cell senescence. However, it is not known how these processes are regulated and initiated in different cell types. Also, the context-dependent interaction partners and binding loci of p53 remain largely elusive. To be able to examine these questions, we here developed knock-in mice expressing triple-FLAG-tagged p53 to facilitate p53 pull-down and tw</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2025-04-04T02:43:55.602Z</modification><creation>2025-04-04T02:43:55.602Z</creation></dates><accession>S-EPMC11445477</accession><cross_references><pubmed>39160273</pubmed><doi>10.1038/s44318-024-00189-z</doi></cross_references></HashMap>