{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pita-Grisanti V"],"funding":["Division of Diabetes, Endocrinology, and Metabolic Diseases","U.S. Department of Veterans Affairs"],"pagination":["316-326"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12823344"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["75(2)"],"pubmed_abstract":["<h4>Article highlights</h4>Mammalian target of rapamycin complex 1 (mTORC1) signaling is essential to β-cell mass, function, and adaptive immunity; however, its specific downstream mediators in type 1 diabetes (T1D) remain poorly defined. We investigated eukaryotic translation initiation factor 4E-binding protein 2 (4E-BP2), a major translational regulator downstream of mTORC1, by using global 4E-BP2-knockout mice on the NOD background. Loss of 4E-BP2 protected male NOD mice from T1D through preservation of β-cell mass and function, coupled with attenuation of autoimmune responses. These findings identify 4E-BP2 as a novel immunometabolic node, highlighting its potential as a therapeutic target for T1D prevention and treatment."],"journal":["Diabetes"],"pubmed_title":["Protection Against Type 1 Diabetes Development in Mice With 4E-BP2 Deletion."],"pmcid":["PMC12823344"],"funding_grant_id":["R01DK133183","R01DK132103","T01BX002728","R01DK138471"],"pubmed_authors":["Pita-Grisanti V","Arenas N","Bayer A","Jaramillo C","Bernal-Mizrachi E","Louzada RA","Blandino-Rosano M","Pecanha FLM"],"additional_accession":[]},"is_claimable":false,"name":"Protection Against Type 1 Diabetes Development in Mice With 4E-BP2 Deletion.","description":"<h4>Article highlights</h4>Mammalian target of rapamycin complex 1 (mTORC1) signaling is essential to β-cell mass, function, and adaptive immunity; however, its specific downstream mediators in type 1 diabetes (T1D) remain poorly defined. We investigated eukaryotic translation initiation factor 4E-binding protein 2 (4E-BP2), a major translational regulator downstream of mTORC1, by using global 4E-BP2-knockout mice on the NOD background. Loss of 4E-BP2 protected male NOD mice from T1D through preservation of β-cell mass and function, coupled with attenuation of autoimmune responses. These findings identify 4E-BP2 as a novel immunometabolic node, highlighting its potential as a therapeutic target for T1D prevention and treatment.","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-06T18:08:28.434Z","creation":"2026-06-04T03:10:31.174Z"},"accession":"S-EPMC12823344","cross_references":{"pubmed":["41236207"],"doi":["10.2337/db25-0348"]}}