{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15"],"submitter":["Li JT"],"pubmed_abstract":["<h4>Background</h4>Glioblastoma (GBM) is the most aggressive and prevalent malignant brain tumor in adults, with poor prognosis despite current therapies. Cyclin-dependent kinase 1 (CDK1), a master regulator of cell cycle progression, has been implicated in oncogenesis, but its downstream phosphorylation network in GBM remains incompletely defined.<h4>Methods</h4>CDK1 expression was examined in clinical GBM tissues and cell lines. Functional studies were performed in U251 cells using CDK1-specific shRNAs. Label-free phosphoproteomic profiling and bioinformatics analyses were conducted to map CDK1-regulated signaling pathways and substrates. Prognostic associations were evaluated using Clinical Proteomic Tumor Analysis Consortium (CPTAC) datasets, and functional assays were used to validate"],"journal":["Frontiers in oncology"],"pagination":["1646698"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12846947"],"repository":["biostudies-literature"],"pubmed_title":["CDK1-driven phosphorylation networks promote glioblastoma progression via MAP1B-mediated microtubule destabilization."],"pmcid":["PMC12846947"],"pubmed_authors":["Li JT","Li MD","Ma CX","Guo YJ","Qian RJ","Li ZX"],"additional_accession":[]},"is_claimable":false,"name":"CDK1-driven phosphorylation networks promote glioblastoma progression via MAP1B-mediated microtubule destabilization.","description":"<h4>Background</h4>Glioblastoma (GBM) is the most aggressive and prevalent malignant brain tumor in adults, with poor prognosis despite current therapies. Cyclin-dependent kinase 1 (CDK1), a master regulator of cell cycle progression, has been implicated in oncogenesis, but its downstream phosphorylation network in GBM remains incompletely defined.<h4>Methods</h4>CDK1 expression was examined in clinical GBM tissues and cell lines. Functional studies were performed in U251 cells using CDK1-specific shRNAs. Label-free phosphoproteomic profiling and bioinformatics analyses were conducted to map CDK1-regulated signaling pathways and substrates. Prognostic associations were evaluated using Clinical Proteomic Tumor Analysis Consortium (CPTAC) datasets, and functional assays were used to validate","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-06-12T03:19:04.953Z","creation":"2026-06-12T03:12:00.226Z"},"accession":"S-EPMC12846947","cross_references":{"pubmed":["41613542"],"doi":["10.3389/fonc.2025.1646698"]}}