{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kohler R"],"funding":["University of Leipzig","Deutsche Forschungsgemeinschaft","Roland-Ernst-Stiftung"],"pagination":["6830-6849"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11229319"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["52(12)"],"pubmed_abstract":["A-MYB (MYBL1) is a transcription factor with a role in meiosis in spermatocytes. The related B-MYB protein is a key oncogene and a master regulator activating late cell cycle genes. To activate genes, B-MYB forms a complex with MuvB and is recruited indirectly to cell cycle genes homology region (CHR) promoter sites of target genes. Activation through the B-MYB-MuvB (MMB) complex is essential for successful mitosis. Here, we discover that A-MYB has a function in transcriptional regulation of the mitotic cell cycle and can substitute for B-MYB. Knockdown experiments in cells not related to spermatogenesis show that B-MYB loss alone merely delays cell cycle progression. Only dual knockdown of B-MYB and A-MYB causes G2/M cell cycle arrest, endoreduplication, and apoptosis. A-MYB can substitut"],"journal":["Nucleic acids research"],"pubmed_title":["A-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation."],"pmcid":["PMC11229319"],"funding_grant_id":["04/22","424870812"],"pubmed_authors":["Kohler R","Engeland K"],"additional_accession":[]},"is_claimable":false,"name":"A-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation.","description":"A-MYB (MYBL1) is a transcription factor with a role in meiosis in spermatocytes. The related B-MYB protein is a key oncogene and a master regulator activating late cell cycle genes. To activate genes, B-MYB forms a complex with MuvB and is recruited indirectly to cell cycle genes homology region (CHR) promoter sites of target genes. Activation through the B-MYB-MuvB (MMB) complex is essential for successful mitosis. Here, we discover that A-MYB has a function in transcriptional regulation of the mitotic cell cycle and can substitute for B-MYB. Knockdown experiments in cells not related to spermatogenesis show that B-MYB loss alone merely delays cell cycle progression. Only dual knockdown of B-MYB and A-MYB causes G2/M cell cycle arrest, endoreduplication, and apoptosis. A-MYB can substitut","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-04-08T19:20:23.459Z","creation":"2025-04-04T11:24:15.186Z"},"accession":"S-EPMC11229319","cross_references":{"pubmed":["38747345"],"doi":["10.1093/nar/gkae370"]}}