{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pathania AS"],"funding":["Pediatric Cancer Research Foundation","Nautica Malibu Triathlon Fund Barbara Mandel Family Fund Helen Dyess Pediatric Cancer Research Fund","U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke","Concern Foundation","NINDS NIH HHS","T.J. Martell Foundation","Harriet H. Samuelsson Foundation"],"pagination":["13902"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6761358"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["G-protein coupled receptor kinase 2 (GRK2; ADRBK1, BARK1) is most known as a regulator of G-protein coupled receptors. However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed "],"journal":["Scientific reports"],"pubmed_title":["GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis."],"pmcid":["PMC6761358"],"funding_grant_id":["NS109751","R21 NS109751","NS094990"],"pubmed_authors":["Ren X","Mahdi MY","Pathania AS","Erdreich-Epstein A","Shackleford GM"],"additional_accession":[]},"is_claimable":false,"name":"GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis.","description":"G-protein coupled receptor kinase 2 (GRK2; ADRBK1, BARK1) is most known as a regulator of G-protein coupled receptors. However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Sep","modification":"2025-04-26T16:47:52.616Z","creation":"2019-10-11T07:11:24Z"},"accession":"S-EPMC6761358","cross_references":{"pubmed":["31554835"],"doi":["10.1038/s41598-019-50157-5"]}}