<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>15</volume><submitter>Li JT</submitter><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</pubmed_abstract><journal>Frontiers in oncology</journal><pagination>1646698</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12846947</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>CDK1-driven phosphorylation networks promote glioblastoma progression via MAP1B-mediated microtubule destabilization.</pubmed_title><pmcid>PMC12846947</pmcid><pubmed_authors>Li JT</pubmed_authors><pubmed_authors>Li MD</pubmed_authors><pubmed_authors>Ma CX</pubmed_authors><pubmed_authors>Guo YJ</pubmed_authors><pubmed_authors>Qian RJ</pubmed_authors><pubmed_authors>Li ZX</pubmed_authors></additional><is_claimable>false</is_claimable><name>CDK1-driven phosphorylation networks promote glioblastoma progression via MAP1B-mediated microtubule destabilization.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-12T03:19:04.953Z</modification><creation>2026-06-12T03:12:00.226Z</creation></dates><accession>S-EPMC12846947</accession><cross_references><pubmed>41613542</pubmed><doi>10.3389/fonc.2025.1646698</doi></cross_references></HashMap>