Publications by authors named "Yuka Yoshidomi"
The interaction between HIV-1 Nef and the Src kinase Hck in macrophages has been shown to accelerate the progression to AIDS. We previously showed that Nef disturbed the N-glycosylation/trafficking of Fms, a cytokine receptor essential for maintaining macrophages in an anti-inflammatory state, in an Hck-dependent manner. Here, we show the underlying molecular mechanism of this effect.
View Article and Find Full Text PDFStem cells in various somatic tissues including hematopoietic stem cells can be identified by the "side population (SP)" phenotype based on the efflux of Hoechst33342. Knockout and enforced expression experiments show that the expression of the Bcrp1/ABCG2 gene is an important determinant of the SP phenotype. In this study, we showed that erythroblasts also express a large amount of Bcrp1/ABCG2.
View Article and Find Full Text PDFArticle Synopsis
- Nef, a protein from HIV-1, interacts with Hck, a kinase found in macrophages, which contributes to AIDS development but how this interaction affects macrophage function is not well understood.
- The study revealed that Nef inhibits the activity of macrophage colony-stimulating factor (M-CSF) by causing a decrease in the surface expression of its receptor, Fms, through a mechanism dependent on Hck.
- Nef causes immature forms of Fms to accumulate in the Golgi apparatus instead of reaching the cell surface, with both the activation of Hck and its localization at the Golgi being crucial for this effect.
Article Synopsis
- M-CSF is a key cytokine that influences the growth and development of monocytes/macrophages, and a new system was created to study its effects on differentiation.
- The study found that while M-CSF typically promotes cell proliferation, the presence of TPA causes a shift toward differentiation, marked by changes in cell shape and increased phagocytic ability.
- When HIV-1 Nef protein is activated in certain cells, it disrupts normal ERK signaling patterns, leading to reduced proliferation and a transient response that hampers the differentiation process linked to prolonged ERK activation.