1,721,031 research outputs found
Lipid raft-dependent FcepsilonRI ubiquitination regulates endocytosis of engaged receptors in mast cells
No full textTyrosine kinase-dependent multiubiquitination of CD16 zeta subunit in human NK cells following receptor engagement
No full textFcepsilonRI engagement induces negative pathways that attenuate receptor-mediated mast cell signalling and functions
No full textSyk kinase activity controls the coupling of engaged FcepsilonRI to the endocytic pathway
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Lipid raft-dependent FcepsilonRI ubiquitination controls endocytosis of engaged receptors in mast cells
No full textUbiquitin and ubiquitin-like modifiers modulate NK cell-mediated recognition and killing of damaged cells
No full textEfficient elimination of transformed and virus-infected cells by natural killer (NK) cells mainly depends on the recognition of "induced self" ligands by activating receptors, including NKG2D and DNAM1. The surface expression of these ligands in stressed or diseased cells results from the integration of transcriptional, post-transcriptional and post-translational mechanisms. Among post-translational mechanisms, recent findings indicate that ubiquitin and ubiquitin-like modifications, namely ubiquitination and SUMOylation, contribute to a very rapid negative regulation of NKG2D and DNAM1 ligand surface expression promoting either ligand degradation or ligand intracellular retention. On the other hand, accumulating evidences demonstrate that NKG2D receptor expression is down-regulated by ubiquitin-dependent endocytosis upon ligand stimulation. In this scenario, the overall consequence of the post-translational modifications of activating NK cell receptors and of their ligands on target cells is to impair effector cell-mediated recognition of damaged cells. Our review summarizes recent findings on the role of post-translational modifications in the modulation of target cell susceptibility to NK cell-mediated killing
Negative signals from FcepsilonRI engagement attenuate receptor-mediated mast cell functions
No full textNegative signal from FcepsilonRI engagement attenuate mast-cell functions.
No full textMast cells have long been recognized as the critical tissue-based effector cells in IgE-mediated allergic diseases. Ligation of the high-affinity receptor for IgE (Fc epsilon RI), constitutively expressed on mast cells, promotes cell activation and immediate release and production of pro-inflammatory mediators. Besides these positive signals, Fc epsilon RI aggregation has recently been understood to generate negative intracellular signals capable of limiting mast cell functional responses. This review is aimed at providing a summary of the mechanisms through which Fc epsilon RI engagement can generate negative signals and regulate mast-cell function. Similar mechanisms are employed by other receptors expressed by immune cells, such as T cell and B cell receptors, pointing to a general concept in negative immunoreceptor signaling
Meccanismi implicati nello spegnimento delle vie di segnalazione mediate dal recettore ad alta affinità per le IgE (FcepsilonRI)
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