{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Beilinson HA"],"funding":["Fondation ARC pour la Recherche sur le Cancer","Yale University","NCATS NIH HHS","University of Pennsylvania","NIAID NIH HHS","Fondation Pasteur Mutualite","National Institutes of Health","NIGMS NIH HHS","La Ligue Contre le Cancer","NIH HHS"],"pagination":["e20210250"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8374863"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["218(10)"],"pubmed_abstract":["Immunoglobulin and T cell receptor gene assembly depends on V(D)J recombination initiated by the RAG1-RAG2 recombinase. The RAG1 N-terminal region (NTR; aa 1-383) has been implicated in regulatory functions whose influence on V(D)J recombination and lymphocyte development in vivo is poorly understood. We generated mice in which RAG1 lacks ubiquitin ligase activity (P326G), the major site of autoubiquitination (K233R), or its first 215 residues (Δ215). While few abnormalities were detected in R1.K233R mice, R1.P326G mice exhibit multiple features indicative of reduced recombination efficiency, including an increased Igκ+:Igλ+ B cell ratio and decreased recombination of Igh, Igκ, Igλ, and Tcrb loci. Previous studies indicate that synapsis of recombining partners during Igh recombination occu"],"journal":["The Journal of experimental medicine"],"pubmed_title":["The RAG1 N-terminal region regulates the efficiency and pathways of synapsis for V(D)J recombination."],"pmcid":["PMC8374863"],"funding_grant_id":["T32 GM-07229","RO1 AI112621","R01 AI112621","T32 AI-007019","R01 AI032524","UL1 TR001863","R21 AI135435","T32 GM007229","T32 AI007019"],"pubmed_authors":["Arya R","Miot C","Beilinson HA","Jones JM","Pongubala JMR","Glynn RA","Xiao J","Yadavalli AD","Saribasak H","Bassing CH","Schatz DG","Bhattacharyya A","Corbett E"],"additional_accession":[]},"is_claimable":false,"name":"The RAG1 N-terminal region regulates the efficiency and pathways of synapsis for V(D)J recombination.","description":"Immunoglobulin and T cell receptor gene assembly depends on V(D)J recombination initiated by the RAG1-RAG2 recombinase. The RAG1 N-terminal region (NTR; aa 1-383) has been implicated in regulatory functions whose influence on V(D)J recombination and lymphocyte development in vivo is poorly understood. We generated mice in which RAG1 lacks ubiquitin ligase activity (P326G), the major site of autoubiquitination (K233R), or its first 215 residues (Δ215). While few abnormalities were detected in R1.K233R mice, R1.P326G mice exhibit multiple features indicative of reduced recombination efficiency, including an increased Igκ+:Igλ+ B cell ratio and decreased recombination of Igh, Igκ, Igλ, and Tcrb loci. Previous studies indicate that synapsis of recombining partners during Igh recombination occu","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2026-06-07T03:20:56.745Z","creation":"2025-05-29T20:30:58.114Z"},"accession":"S-EPMC8374863","cross_references":{"pubmed":["34402853"],"doi":["10.1084/jem.20210250"]}}