{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Thompson PK"],"funding":["NIAID NIH HHS","Gouvernement du Canada | Canadian Institutes of Health Research","CIHR","Canadian Cancer Society Research Institute"],"pagination":["77-92"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9248976"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["209(1)"],"pubmed_abstract":["The zinc-finger transcription factor GATA-3 plays a crucial role during early T cell development and also dictates later T cell differentiation outcomes. However, its role and collaboration with the Notch signaling pathway in the induction of T lineage specification and commitment have not been fully elucidated. We show that GATA-3 deficiency in mouse hematopoietic progenitors results in an early block in T cell development despite the presence of Notch signals, with a failure to upregulate Bcl11b expression, leading to a diversion along a myeloid, but not a B cell, lineage fate. GATA-3 deficiency in the presence of Notch signaling results in the apoptosis of early T lineage cells, as seen with inhibition of CDK4/6 (cyclin-dependent kinases 4 and 6) function, and dysregulated cyclin-depend"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Realization of the T Lineage Program Involves GATA-3 Induction of Bcl11b and Repression of Cdkn2b Expression."],"pmcid":["PMC9248976"],"funding_grant_id":["P01 AI102853","MOP-119538","FDN-154332"],"pubmed_authors":["Iscove NN","Leid M","Zuniga-Pflucker JC","Vogel WK","Anderson MK","Thompson PK","Shah DK","Venables T","Chen ELY","Frelin C","Lee CR","de Pooter RF"],"additional_accession":[]},"is_claimable":false,"name":"Realization of the T Lineage Program Involves GATA-3 Induction of Bcl11b and Repression of Cdkn2b Expression.","description":"The zinc-finger transcription factor GATA-3 plays a crucial role during early T cell development and also dictates later T cell differentiation outcomes. However, its role and collaboration with the Notch signaling pathway in the induction of T lineage specification and commitment have not been fully elucidated. We show that GATA-3 deficiency in mouse hematopoietic progenitors results in an early block in T cell development despite the presence of Notch signals, with a failure to upregulate Bcl11b expression, leading to a diversion along a myeloid, but not a B cell, lineage fate. GATA-3 deficiency in the presence of Notch signaling results in the apoptosis of early T lineage cells, as seen with inhibition of CDK4/6 (cyclin-dependent kinases 4 and 6) function, and dysregulated cyclin-depend","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2026-05-27T21:03:45.562Z","creation":"2025-02-18T22:34:18.8Z"},"accession":"S-EPMC9248976","cross_references":{"pubmed":["35705252"],"doi":["10.4049/jimmunol.2100366"]}}