{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hesselson D"],"funding":["NIDDK NIH HHS"],"pagination":["712-7"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3081919"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(8)"],"pubmed_abstract":["Pluripotent embryonic cells become progressively lineage restricted during development in a process that culminates in the differentiation of stable organ-specific cell types that perform specialized functions. Terminally differentiated pancreatic acinar cells do not have the innate capacity to contribute to the endocrine β cell lineage, which is destroyed in individuals with autoimmune diabetes. Some cell types can be reprogrammed using a single factor, whereas other cell types require continuous activity of transcriptional regulators to repress alternate cell fates. Thus, we hypothesized that a transcriptional network continuously maintains the pancreatic acinar cell fate. We found that postembryonic antagonism of Ptf1a, a master regulator of pancreatic development and acinar cell fate s"],"journal":["Current biology : CB"],"pubmed_title":["Suppression of Ptf1a activity induces acinar-to-endocrine conversion."],"pmcid":["PMC3081919"],"funding_grant_id":["DK075032","R01 DK075032-04","R01 DK075032-05","R01 DK075032","R01 DK075032-04S1"],"pubmed_authors":["Stainier DY","Hesselson D","Anderson RM"],"additional_accession":[]},"is_claimable":false,"name":"Suppression of Ptf1a activity induces acinar-to-endocrine conversion.","description":"Pluripotent embryonic cells become progressively lineage restricted during development in a process that culminates in the differentiation of stable organ-specific cell types that perform specialized functions. Terminally differentiated pancreatic acinar cells do not have the innate capacity to contribute to the endocrine β cell lineage, which is destroyed in individuals with autoimmune diabetes. Some cell types can be reprogrammed using a single factor, whereas other cell types require continuous activity of transcriptional regulators to repress alternate cell fates. Thus, we hypothesized that a transcriptional network continuously maintains the pancreatic acinar cell fate. We found that postembryonic antagonism of Ptf1a, a master regulator of pancreatic development and acinar cell fate s","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Apr","modification":"2025-04-25T21:49:56.04Z","creation":"2019-03-27T00:40:55Z"},"accession":"S-EPMC3081919","cross_references":{"pubmed":["21497092"],"doi":["10.1016/j.cub.2011.03.041"]}}