6533b86efe1ef96bd12cbffb
RESEARCH PRODUCT
Lack of NFATc1 SUMOylation prevents autoimmunity and alloreactivity
Martin VaethIngolf BerberichMathias ButtmannAnika KönigSubrahmanya D VallabhapurapuLena DietzMatthias KleinAndreas BeilhackChunguang LiangAndreas RosenwaldYin XiaoMusga QureischiTobias BoppStefan Klein-hesslingAnja MottokEdgar SerflingFriederike Berberich-siebeltsubject
0301 basic medicineProtein sumoylationEncephalomyelitis Autoimmune ExperimentalT cellStem Cells & RegenerationImmunologySUMO proteinAutoimmunityBiologyenvironment and public healthT-Lymphocytes RegulatoryArticleMinor Histocompatibility AntigensMice03 medical and health sciences0302 clinical medicineImmune systemNeuroinflammationAldesleukinSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyTranscription factorMice Knockoutintegumentary systemNFATC Transcription FactorsExperimental autoimmune encephalomyelitisSumoylationNFATmedicine.diseaseCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologymedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCytokinesPositive Regulatory Domain I-Binding Factor 1description
A novel transgenic mouse, in which the transcription factor NFATc1 bears lysine-to-arginine mutations that prevent modification by SUMO, develops normally and is healthy. However, SUMO-insensitive NFATc1 transmits strong tolerogenic signals, thus preventing autoimmune and alloimmune T cell responses.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2020-09-28 | Journal of Experimental Medicine |