{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dutt P"],"funding":["Canadian Government | Canadian Institutes of Health Research","Canadian Government | Canadian Institutes of Health Research (CIHR)"],"pagination":["e2300606121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11087748"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(19)"],"pubmed_abstract":["β-catenin has influential roles affecting embryonic development, tissue homeostasis, and human diseases including cancer. Cellular β-catenin levels are exquisitely controlled by a variety of regulatory mechanisms. In the course of exploring the functions of the Nek10 tyrosine kinase, we observed that deletion of Nek10 in lung adenocarcinoma cells resulted in dramatic stabilization of β-catenin, suggestive of a Nek10 role in the control of β-catenin turnover. Nek10-deficient cells exhibited diminished ability to form tumorspheres in suspension, grow in soft agar, and colonize mouse lung tissue following tail vein injection. Mechanistically, Nek10 associates with the Axin complex, responsible for β-catenin degradation, where it phosphorylates β-catenin at Tyr30, located within the regulatory"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["β-catenin turnover is regulated by Nek10-mediated tyrosine phosphorylation in A549 lung adenocarcinoma cells."],"pmcid":["PMC11087748"],"funding_grant_id":["174994"],"pubmed_authors":["Podmore L","Dutt P","Haider N","Mouaaz S","Stambolic V"],"additional_accession":[]},"is_claimable":false,"name":"β-catenin turnover is regulated by Nek10-mediated tyrosine phosphorylation in A549 lung adenocarcinoma cells.","description":"β-catenin has influential roles affecting embryonic development, tissue homeostasis, and human diseases including cancer. Cellular β-catenin levels are exquisitely controlled by a variety of regulatory mechanisms. In the course of exploring the functions of the Nek10 tyrosine kinase, we observed that deletion of Nek10 in lung adenocarcinoma cells resulted in dramatic stabilization of β-catenin, suggestive of a Nek10 role in the control of β-catenin turnover. Nek10-deficient cells exhibited diminished ability to form tumorspheres in suspension, grow in soft agar, and colonize mouse lung tissue following tail vein injection. Mechanistically, Nek10 associates with the Axin complex, responsible for β-catenin degradation, where it phosphorylates β-catenin at Tyr30, located within the regulatory","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-01T17:29:05.523Z","creation":"2026-04-08T14:16:40.78Z"},"accession":"S-EPMC11087748","cross_references":{"pubmed":["38683979"],"doi":["10.1073/pnas.2300606121"]}}