Figure 4
A CTCL signaling network affected by somatic mutations. Schematic representation showing key T-cell signaling pathways harboring by mutations in this study. These signaling pathways are tightly regulated and can be activated by downstream signals elicited by the interaction at the extracellular membrane of soluble ligands or cell antigens with their cognate receptors, such as TCR, CCR4, TGFB-R, TLRs, and IL6-ST. These have been shown to potentiate the activity of transcription factors such as E2A, NFAT, NFkB, and STAT3, which, in turn, have been shown participate in essential T-cell activities including cell proliferation and survival, as well as differentiation processes toward the acquisition of specific T cell lineages. For clarity, only a selection of the genes found to be mutated in our study are highlighted (gray rectangles) and represented in the scheme in which we think they can participate in this T-cell signaling network.

A CTCL signaling network affected by somatic mutations. Schematic representation showing key T-cell signaling pathways harboring by mutations in this study. These signaling pathways are tightly regulated and can be activated by downstream signals elicited by the interaction at the extracellular membrane of soluble ligands or cell antigens with their cognate receptors, such as TCR, CCR4, TGFB-R, TLRs, and IL6-ST. These have been shown to potentiate the activity of transcription factors such as E2A, NFAT, NFkB, and STAT3, which, in turn, have been shown participate in essential T-cell activities including cell proliferation and survival, as well as differentiation processes toward the acquisition of specific T cell lineages. For clarity, only a selection of the genes found to be mutated in our study are highlighted (gray rectangles) and represented in the scheme in which we think they can participate in this T-cell signaling network.

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