{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Martino F"],"funding":["Associazione Italiana per la Ricerca sul Cancro","Ministero della Salute","Ministero della Salute Ricerca Corrente: 2024-2025","European Research Council","Italian Ministry of University and Scientific Research grant PRIN 2020","FPRC 5xmille Ministero Salute 2020","Fondazione Piemontese per la Ricerca sul Cancro, FPRC 5xmille Ministero Salute 2017 PTCRC-INTRA 2020"],"pagination":["e02269"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12631847"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(43)"],"pubmed_abstract":["TBC1D22B is a GTPase-activating protein (GAP) associated with poor prognosis in breast cancer (BC). Using complementary proximity-labeling and co-immunoprecipitation proteomics, the TBC1D22B interactome in BC cells is defined, revealing strong enrichment in components of the ER-to-Golgi trafficking machinery, endosomal transport, and adhesion-related pathways. Functional assays, using the Retention Using Selective Hooks (RUSH) system, demonstrate that TBC1D22B inhibits ER-to-Golgi transport in a GAP-dependent manner. Mechanistic studies identify RAB1B as a direct target of TBC1D22B, and RAB1B silencing phenocopies the trafficking defects caused by TBC1D22B overexpression. In 3D culture, TBC1D22B promotes spheroid growth in a manner dependent on its GAP activity and not replicated by its pa"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["TBC1D22B Regulates ER-to-Golgi Trafficking via RAB1B Inactivation and Promotes Oncogenic Programs in Breast Cancer."],"pmcid":["PMC12631847"],"funding_grant_id":["22811","PRO-ACTIVE","PNRR-MCNT2-2023-12378490 Next Generation EU","2020R2BP2E","ERC-CoG2020 101002280","2022W93FTW","projectSEE-HER","101002280","24415"],"pubmed_authors":["Martino F","Freddi S","Murabito A","Pennisi R","Bussolino F","Bedin F","Matoskova B","Boncompain G","Sigismund S","Lanzetti L","Cuomo A","Lupi M","Fontana S","Fardin A","Perez F","Villari G","Andreoli L"],"additional_accession":[]},"is_claimable":false,"name":"TBC1D22B Regulates ER-to-Golgi Trafficking via RAB1B Inactivation and Promotes Oncogenic Programs in Breast Cancer.","description":"TBC1D22B is a GTPase-activating protein (GAP) associated with poor prognosis in breast cancer (BC). Using complementary proximity-labeling and co-immunoprecipitation proteomics, the TBC1D22B interactome in BC cells is defined, revealing strong enrichment in components of the ER-to-Golgi trafficking machinery, endosomal transport, and adhesion-related pathways. Functional assays, using the Retention Using Selective Hooks (RUSH) system, demonstrate that TBC1D22B inhibits ER-to-Golgi transport in a GAP-dependent manner. Mechanistic studies identify RAB1B as a direct target of TBC1D22B, and RAB1B silencing phenocopies the trafficking defects caused by TBC1D22B overexpression. In 3D culture, TBC1D22B promotes spheroid growth in a manner dependent on its GAP activity and not replicated by its pa","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T17:21:29.812Z","creation":"2026-05-19T03:11:57.39Z"},"accession":"S-EPMC12631847","cross_references":{"pubmed":["40878439"],"doi":["10.1002/advs.202502269"]}}