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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Targeting CLL-1 for acute myeloid leukemia therapy

Fig. 2

Mechanism of CLL-1 function. The ligands from dead cell or other material trigger the phosphorylation of ITAM and activation of Syk signaling, eliciting the production of reactive oxygen species (ROS) and activation of NF-kB through a complex containing CARD9, MALT1, and Bcl-10; the latter leads to the gene transcription and release of chemokines/cytokines, facilitating neutrophil activation and inflammatory infiltration. This process can be counterbalanced when MSU or unknown ligand on dead cells bind CLL-1, recruiting tyrosine phosphatases SHP-1, and SHP-2 to negatively regulate Syk signaling, as a result, inflammation is eliminated or alleviated. It is unknown whether YXXM in CLL-1 can bind P85 of PI3K and activate the downstream signals

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