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Figure 8 | BMC Microbiology

Figure 8

From: c-KIT signaling is targeted by pathogenic Yersiniato suppress the host immune response

Figure 8

Schematic of multiple signaling pathways induced by extracellular stimuli to activate transcription factors that regulate the pro-inflammatory cell response. Cell surface receptors translate ligand binding into activation of host intracellular signaling pathways. The genes depicted in grey were identified in the RNAi screen in which gene silencing counteracted Yersinia-mediated inhibition of NF-κB activation in response to TNF-α. Cell stimuli, such as stem cell factor (SCF, black triangle), the natural ligand of c-KIT, initiate cell signaling that converge on the activation of two key transcription factors NF-κB and EGR1. Bolded triangles depict interactions between Yersinia Yop effectors and host signaling proteins. The cartoon includes primary signaling molecules and is not a comprehensive description of all known players or feedback mechanisms in these signaling pathways.

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