Extended Data Fig. 10: Working model for NOD1-controlled STAT5-medaited lymphopoiesis.
From: Microbial ligand-independent regulation of lymphopoiesis by NOD1
The diagram depicts the proposed role of NOD1 in the STAT5 signaling pathway downstream of lymphopoietic cytokine receptors in the three different mouse genotypes studied here. In the case of WT mice (a) cytokine receptor engagement triggers phosphorylation and dimerization of STAT5, which are facilitated by NOD1, resulting in optimal STAT5 nuclear translocation followed by induction of lymphopoiesis. In mice lacking the entire NOD1 protein (b) STAT5 phosphorylation is decreased, fewer p-STAT5 dimers are formed, and although nuclear translocation is not affected, the STAT5-mediation signal is diminished. In mice that express ΔCARD NOD1 (c) both the STAT5 phosphorylation and its nuclear translocation are impaired, resulting in an even lower lymphopoietic cytokine output.
