{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Almeida FF"],"funding":["LOEWE Center for Cell and Gene Therapy Germany","National Health and Medical Research Council Australia","GOIN postdoc fellowship Frankfurt Germany"],"pagination":["e1475875"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6169588"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(10)"],"pubmed_abstract":["NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCR<sup>B6C14R</sup> strain. Ly5.1<sup>C14R</sup> NK cells expressed similar levels of <i>Ncr1</i> mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors <i>in vivo</i>. Expression of the mutant NKp46<sup>C14R</sup> in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1<sup>C14R</sup> mice had normal number of NK cells, t"],"journal":["Oncoimmunology"],"pubmed_title":["A point mutation in the <i>Ncr1</i> signal peptide impairs the development of innate lymphoid cell subsets."],"pmcid":["PMC6169588"],"funding_grant_id":["PCOFUND-GA-2011-291776","1054925","1124907","III L 4-518/17.004"],"pubmed_authors":["Ullrich E","Marcais A","Schleicher U","Ugolini S","Kalensee F","Almeida FF","Shi W","Firth M","Herold MJ","Koch J","Willis SN","Luong K","Zoller T","Galluso J","Liao Y","Belz GT","Giannattasio A","Mercier FE","Spallotta F","Kueh AJ","Narni-Mancinelli E","Walzer T","Rais B","Weil S","Faure F","Tognarelli S","Scadden DT","Steinle A","Huntington ND","Chiocchetti AG","Friede ME","Vivier E"],"additional_accession":[]},"is_claimable":false,"name":"A point mutation in the <i>Ncr1</i> signal peptide impairs the development of innate lymphoid cell subsets.","description":"NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCR<sup>B6C14R</sup> strain. Ly5.1<sup>C14R</sup> NK cells expressed similar levels of <i>Ncr1</i> mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors <i>in vivo</i>. Expression of the mutant NKp46<sup>C14R</sup> in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1<sup>C14R</sup> mice had normal number of NK cells, t","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018","modification":"2026-04-30T22:40:29.397Z","creation":"2019-03-26T23:59:12Z"},"accession":"S-EPMC6169588","cross_references":{"pubmed":["30288342"],"doi":["10.1080/2162402X.2018.1475875"]}}