http://purl.uniprot.org/citations/36761164 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/36761164 | http://www.w3.org/2000/01/rdf-schema#comment | "G-protein coupled receptors (GPCR) regulate 3',5'-cyclic adenosine monophosphate (cAMP) levels in T cells. cAMP as ubiquitous second messenger is crucial for adequate physiology of T cells by mediating effector T cell (Teff) function as well as regulatory T cell (Treg)-mediated immunosuppression. Several GPCRs have been identified to be crucial for Teff and Treg function. However, the role of the orphan, constitutively active Gs-coupled GPCR GPR52 is unknown. Here we show that GPR52 regulates cAMP levels in T cells but does not affect T cell function. We found that stimulation of transfected HEK cells or primary T cells with a GPR52 agonist results in a rise of intracellular cAMP. However, neither Gpr52 deficiency nor pharmacological modulation of GPR52 by antagonists or agonists affected T cell activation, differentiation, and proliferation or Treg-mediated immunosuppression. Moreover, Gpr52 deletion did not modify the clinical disease course of experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that a modulation of cAMP levels in T cells does not inevitably result in altered T cell function. While we could not identify an obvious role of GPR52 in in vitro T cell assays and in vivo CNS autoimmunity, it might regulate T cell function in a different context or affect the function of other GPR52-expressing cells."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.org/dc/terms/identifier | "doi:10.3389/fimmu.2022.1113348"xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Bauer S."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Engler J.B."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Friese M.A."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Nikolaev V.O."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Sonner J.K."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Kurelic R."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Krieg P.F."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/author | "Scharenberg M.F."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/name | "Front Immunol"xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/pages | "1113348"xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/title | "GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses."xsd:string |
http://purl.uniprot.org/citations/36761164 | http://purl.uniprot.org/core/volume | "13"xsd:string |
http://purl.uniprot.org/citations/36761164 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/36761164 |
http://purl.uniprot.org/citations/36761164 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/36761164 |
http://purl.uniprot.org/uniprot/#_P0C5J4-mappedCitation-36761164 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/36761164 |
http://purl.uniprot.org/uniprot/P0C5J4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/36761164 |