Publications by authors named "Federica Seydel"
Article Synopsis
- The study examines how STAT5, a signaling protein, misbinds to genes involved in inflammation in monocytes from Type 1 diabetic humans.
- Researchers used genetically modified mice (B6.NOD C11bxC1tb) to model these changes, demonstrating that specific genetic regions combined with STAT5 binding lead to altered expression of inflammatory genes CSF2 and PTGS2.
- These modified mice showed symptoms of diabetes, such as high blood sugar and pancreatic damage, suggesting that the gene expression changes in immune cells may increase diabetes risk even in mice that are not typically prone to autoimmune diseases.
STAT5 proteins are adaptor proteins for histone acetylation enzymes. Histone acetylation at promoter and enhancer chromosomal regions opens the chromatin and allows access of transcription enzymes to specific genes in rapid response cell signals, such as in inflammation. Histone acetylation-mediated gene regulation is involved in expression of 2 key inflammatory response genes: CSF2, encoding granulocyte-macrophage colony stimulating factor (GM-CSF), and PTGS2, encoding prostaglandin synthase 2/cyclooxygenase 2 (PGS2/COX2).
View Article and Find Full Text PDFSpecific proteins are concentrated within primary cilia, whereas others remain excluded. To understand the mechanistic basis of entry into cilia, we developed an in vitro assay using cells in which the plasma membrane was permeabilized, but the ciliary membrane was left intact. Using a diffusion-to-capture system and quantitative analysis, we find that proteins >9 nm in diameter (∼100 kD) are restricted from entering cilia, and we confirm these findings in vivo.
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