{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["301(1)"],"submitter":["Yasutake R"],"funding":["Japan Society for the Promotion of Science"],"pubmed_abstract":["Ephexin proteins are guanine nucleotide exchange factors for the Rho GTPases. We reported that Ephexin4 regulates M-phase progression downstream of phosphorylated EphA2, a receptor-type tyrosine kinase, through RhoG activation; however, the regulation of Ephexin4 during M phase remains unknown. In this study, a novel Ephexin4 phosphorylation site was identified at Ser41, exclusively in M phase. Ephexin4 knockdown prolonged the duration of M phase by activating the spindle assembly checkpoint, at which BubR1 was localized at the kinetochores of the misaligned chromosomes. This delay was alleviated by re-expression of wild-type, but not S41A Ephexin4. The Ephexin4 knockdown caused chromosome misalignment and reduced the RhoG localization to the plasma membrane. These phenotypes were rescued "],"journal":["The Journal of biological chemistry"],"pagination":["108084"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11758948"],"repository":["biostudies-literature"],"pubmed_title":["Phosphorylation of Ephexin4 at Ser-41 contributes to chromosome alignment via RhoG activation in cell division."],"pmcid":["PMC11758948"],"pubmed_authors":["Kuwajima H","Yasutake R","Nakayama Y","Saito Y","Tanaka J","Yuki R"],"additional_accession":[]},"is_claimable":false,"name":"Phosphorylation of Ephexin4 at Ser-41 contributes to chromosome alignment via RhoG activation in cell division.","description":"Ephexin proteins are guanine nucleotide exchange factors for the Rho GTPases. We reported that Ephexin4 regulates M-phase progression downstream of phosphorylated EphA2, a receptor-type tyrosine kinase, through RhoG activation; however, the regulation of Ephexin4 during M phase remains unknown. In this study, a novel Ephexin4 phosphorylation site was identified at Ser41, exclusively in M phase. Ephexin4 knockdown prolonged the duration of M phase by activating the spindle assembly checkpoint, at which BubR1 was localized at the kinetochores of the misaligned chromosomes. This delay was alleviated by re-expression of wild-type, but not S41A Ephexin4. The Ephexin4 knockdown caused chromosome misalignment and reduced the RhoG localization to the plasma membrane. These phenotypes were rescued ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2025-04-03T23:36:49.015Z","creation":"2025-04-03T23:36:49.015Z"},"accession":"S-EPMC11758948","cross_references":{"pubmed":["39675713"],"doi":["10.1016/j.jbc.2024.108084"]}}