{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xufeng R"],"funding":["NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS"],"pagination":["27-32"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8974940"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2(1)"],"pubmed_abstract":["The RNA editing enzyme ADAR1 has been shown to be an essential molecule for hematopoietic cell differentiation, embryonic development, and regulation of immune responses. Here, we present evidence in a T-cell-specific gene knockout mouse model that ADAR1 is required for early T cell development. Loss of ADAR1 led to cell death of the progenitors at the double negative stage and prevented T cell maturation in the thymus. Furthermore, ADAR1 deletion in pre-T cells preferentially affected TCRβ-expressing cells causing TCRβ positive cell depletion. Interruption of IFN signaling occurred in the premature T cells, indicating a role of IFN signaling in the survival of TCRβ-expressing cells regulated by ADAR1. This study demonstrated an essential role for the RNA editing enzyme ADAR1 as a potential regulator for T-cell fate determination during clonal selection, which, in turn, contributes to immunologic homeostasis."],"journal":["Blood science (Baltimore, Md.)"],"pubmed_title":["RNA editing enzyme ADAR1 is required for early T cell development."],"pmcid":["PMC8974940"],"funding_grant_id":["R01 HL070561","R21 AI078094","R21 CA158650"],"pubmed_authors":["Cheng T","Nie D","Wang Q","Xufeng R","Wang W","Yang Q"],"additional_accession":[]},"is_claimable":false,"name":"RNA editing enzyme ADAR1 is required for early T cell development.","description":"The RNA editing enzyme ADAR1 has been shown to be an essential molecule for hematopoietic cell differentiation, embryonic development, and regulation of immune responses. Here, we present evidence in a T-cell-specific gene knockout mouse model that ADAR1 is required for early T cell development. Loss of ADAR1 led to cell death of the progenitors at the double negative stage and prevented T cell maturation in the thymus. Furthermore, ADAR1 deletion in pre-T cells preferentially affected TCRβ-expressing cells causing TCRβ positive cell depletion. Interruption of IFN signaling occurred in the premature T cells, indicating a role of IFN signaling in the survival of TCRβ-expressing cells regulated by ADAR1. This study demonstrated an essential role for the RNA editing enzyme ADAR1 as a potential regulator for T-cell fate determination during clonal selection, which, in turn, contributes to immunologic homeostasis.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jan","modification":"2025-04-19T12:57:30.315Z","creation":"2025-04-19T12:57:30.315Z"},"accession":"S-EPMC8974940","cross_references":{"pubmed":["35399867"],"doi":["10.1097/BS9.0000000000000039"]}}