{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nandagopal S"],"funding":["National Institutes of Health","National Institute of General Medical Sciences","Damon Runyon Cancer Research Foundation","NIGMS NIH HHS"],"pagination":["115077"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11774475"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["43(12)"],"pubmed_abstract":["Stem cells integrate multiple environmental signals to activate appropriate fate programs. To ensure coherent responses, alternative fates must be concomitantly inactivated. However, mechanisms that coordinate fates in a signal-specific manner are not fully understood. Here, we investigate the role of a network of basic-helix-loop-helix (bHLH) transcription factors in neural stem cells, which integrate leukemia inhibitory factor (LIF) and bone morphogenetic protein (BMP) signaling to synergistically induce glial fibrillary acidic protein (GFAP), a key astrocyte-fate determinant. Using quantitative RNA-fluorescence in situ hybridization (FISH) and ectopic expression, we find that multiple bHLHs that promote alternative fates also repress GFAP but are all suppressed by BMP and, to a lesser e"],"journal":["Cell reports"],"pubmed_title":["Activation-derepression synergy enables a bHLH network to coordinate a signal-specific fate response."],"pmcid":["PMC11774475"],"funding_grant_id":["K99 GM151398","DRG-2339-18","R35 GM139572","1K99GM151398"],"pubmed_authors":["Terrio A","Vicente FZ","Lahav G","Nandagopal S","Megason SG","Jambhekar A"],"additional_accession":[]},"is_claimable":false,"name":"Activation-derepression synergy enables a bHLH network to coordinate a signal-specific fate response.","description":"Stem cells integrate multiple environmental signals to activate appropriate fate programs. To ensure coherent responses, alternative fates must be concomitantly inactivated. However, mechanisms that coordinate fates in a signal-specific manner are not fully understood. Here, we investigate the role of a network of basic-helix-loop-helix (bHLH) transcription factors in neural stem cells, which integrate leukemia inhibitory factor (LIF) and bone morphogenetic protein (BMP) signaling to synergistically induce glial fibrillary acidic protein (GFAP), a key astrocyte-fate determinant. Using quantitative RNA-fluorescence in situ hybridization (FISH) and ectopic expression, we find that multiple bHLHs that promote alternative fates also repress GFAP but are all suppressed by BMP and, to a lesser e","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2026-05-29T14:18:18.842Z","creation":"2025-04-04T22:24:31.118Z"},"accession":"S-EPMC11774475","cross_references":{"pubmed":["39671287"],"doi":["10.1016/j.celrep.2024.115077"]}}