A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

@inproceedings{Almeida2018APM,
  title={A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets},
  author={Francisca F Almeida and Sara Tognarelli and Antoine Marçais and Andrew Jing Yaw Kueh and Miriam E. Friede and Yang Kai Liao and Simon N. Willis and Kylie Luong and Fabrice Faure and François E. Mercier and Justine Galluso and Matthew A. Firth and Emilie Narni-Mancinelli and Bushra Rais and David T. Scadden and Francesco Spallotta and Sandra Weil and Ariane Giannattasio and Franziska Kalensee and Tobias Z{\"o}ller and Nicholas D Huntington and Ulrike Schleicher and Andreas G Chiocchetti and Sophie Ugolini and M. Jerosch Herold and Wei Min Shi and Joachim Koch and Alexander Steinle and Eric Vivier and Thierry Walzer and Gabrielle T. Belz and Evelyn Ullrich},
  booktitle={Oncoimmunology},
  year={2018}
}
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 NCRB6C14R strain. Ly5.1C14R NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface… CONTINUE READING
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