<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>22(4)</volume><submitter>Palmieri M</submitter><funding>National Health and Medical Research Council</funding><pubmed_abstract>The canonical view of PI3Kα signaling describes phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P&lt;sub>3&lt;/sub>) generation and activation of downstream effectors at the plasma membrane or at microtubule-bound endosomes. Here, we show that colorectal cancer (CRC) cell lines exhibit a diverse plasma membrane-nuclear distribution of PI3Kα, controlling corresponding levels of subcellular PtdIns(3,4,5)P&lt;sub>3&lt;/sub> pools. PI3Kα nuclear translocation was mediated by the importin β-dependent nuclear import pathway. By PtdIns(3,4,5)P&lt;sub>3&lt;/sub> affinity capture mass spectrometry done in the presence of SDS on CRC cell lines with PI3Kα nuclear localization, we identified 867 potential nuclear PtdIns(3,4,5)P&lt;sub>3&lt;/sub> effector proteins. Nuclear PtdIns(3,4,5)P&lt;sub>3&lt;/sub> interactome protein</pubmed_abstract><journal>Molecular &amp; cellular proteomics : MCP</journal><pagination>100529</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10130476</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>PI3Kα Translocation Mediates Nuclear PtdIns(3,4,5)P&lt;sub>3&lt;/sub> Effector Signaling in Colorectal Cancer.</pubmed_title><pmcid>PMC10130476</pmcid><pubmed_authors>Sieber OM</pubmed_authors><pubmed_authors>Mouradov D</pubmed_authors><pubmed_authors>Nowell CJ</pubmed_authors><pubmed_authors>Desai J</pubmed_authors><pubmed_authors>Catimel B</pubmed_authors><pubmed_authors>Palmieri M</pubmed_authors><pubmed_authors>Christie M</pubmed_authors><pubmed_authors>Sakthianandeswaren A</pubmed_authors><pubmed_authors>Williamson NA</pubmed_authors><pubmed_authors>Burgess AW</pubmed_authors><pubmed_authors>Gibbs P</pubmed_authors><pubmed_authors>Kapp E</pubmed_authors><pubmed_authors>Ang CS</pubmed_authors></additional><is_claimable>false</is_claimable><name>PI3Kα Translocation Mediates Nuclear PtdIns(3,4,5)P&lt;sub>3&lt;/sub> Effector Signaling in Colorectal Cancer.</name><description>The canonical view of PI3Kα signaling describes phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P&lt;sub>3&lt;/sub>) generation and activation of downstream effectors at the plasma membrane or at microtubule-bound endosomes. Here, we show that colorectal cancer (CRC) cell lines exhibit a diverse plasma membrane-nuclear distribution of PI3Kα, controlling corresponding levels of subcellular PtdIns(3,4,5)P&lt;sub>3&lt;/sub> pools. PI3Kα nuclear translocation was mediated by the importin β-dependent nuclear import pathway. By PtdIns(3,4,5)P&lt;sub>3&lt;/sub> affinity capture mass spectrometry done in the presence of SDS on CRC cell lines with PI3Kα nuclear localization, we identified 867 potential nuclear PtdIns(3,4,5)P&lt;sub>3&lt;/sub> effector proteins. Nuclear PtdIns(3,4,5)P&lt;sub>3&lt;/sub> interactome protein</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-07-14T21:05:15.349Z</modification><creation>2025-04-04T20:20:14.159Z</creation></dates><accession>S-EPMC10130476</accession><cross_references><pubmed>36931626</pubmed><doi>10.1016/j.mcpro.2023.100529</doi></cross_references></HashMap>