Enhanced c-Fms/M-CSF Receptor Signaling and Wound-Healing Process in Bone Marrow-Derived Macrophages of Signal-Transducing Adaptor Protein-2 (STAP-2) Deficient Mice
Copyright policy )Enhanced c-Fms/M-CSF Receptor Signaling and Wound-Healing Process in Bone Marrow-Derived Macrophages of Signal-Transducing Adaptor Protein-2 (STAP-2) Deficient Mice
Signal-transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein as a c-Fms/M-CSF receptor-interacting protein and constitutively expressed in macrophages. In our previous study, we examined the role of STAP-2 in the c-Fms/M-CSF receptor signaling using a murine macrophage tumor cells line, Raw264.7. Overexpression of STAP-2 in Raw264.7 cells markedly suppressed M-CSF-induced activation of extracellular signal regulated kinase and Akt. In addition, Raw264.7 overexpressing STAP-2 affected cell migration in wound-healing process. These results suggest that STAP-2 deficiency influences endogenous c-Fms/M-CSF receptor signaling. Here we show that loss of STAP-2 expression in knockout mouse macrophages results in marked enhancement of the c-Fms/M-CSF receptor signaling and wound-healing process. We therefore propose that STAP-2 acts as an endogenous regulator in normal macrophages functions.
Mice, Knockout, Wound Healing, Macrophages, Blotting, Western, Receptor, Macrophage Colony-Stimulating Factor, macrophage, wound-healing, Flow Cytometry, M-CSF, Recombinant Proteins, 499, c-Fms, Oncogene Protein v-akt, Mice, Cell Movement, Animals, Humans, Extracellular Signal-Regulated MAP Kinases, signal-transducing adaptor protein-2, Adaptor Proteins, Signal Transducing, Cell Proliferation, Signal Transduction
Mice, Knockout, Wound Healing, Macrophages, Blotting, Western, Receptor, Macrophage Colony-Stimulating Factor, macrophage, wound-healing, Flow Cytometry, M-CSF, Recombinant Proteins, 499, c-Fms, Oncogene Protein v-akt, Mice, Cell Movement, Animals, Humans, Extracellular Signal-Regulated MAP Kinases, signal-transducing adaptor protein-2, Adaptor Proteins, Signal Transducing, Cell Proliferation, Signal Transduction
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