24 results on '"Peeters, Janneke G. C."'
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2. A PRC1–RNF2 knockout punch for cancer
3. Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition
4. Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition.
5. Increased autophagy contributes to the inflammatory phenotype of juvenile idiopathic arthritis synovial fluid T cells
6. Review: Enhancers in Autoimmune Arthritis: Implications and Therapeutic Potential
7. Conserved human effector Treg cell transcriptomic and epigenetic signature in arthritic joint inflammation
8. Restoring T Cell Tolerance, Exploring the Potential of Histone Deacetylase Inhibitors for the Treatment of Juvenile Idiopathic Arthritis
9. SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis
10. Enhancers in autoimmune arthritis : Implications and therapeutic potential
11. Increased autophagy contributes to the inflammatory phenotype of juvenile idiopathic arthritis synovial fluid T cells
12. Enhancers in autoimmune arthritis: Implications and therapeutic potential
13. Autoimmune disease-associated gene expression is reduced by BET-inhibition
14. Autoimmune disease-associated gene expression is reduced by BET-inhibition
15. Inhibition of Super-Enhancer Activity in Autoinflammatory Site-Derived T Cells Reduces Disease-Associated Gene Expression
16. Inhibition of Super-Enhancer Activity in Autoinflammatory Site-Derived T Cells Reduces Disease-Associated Gene Expression
17. Site-Specific Chemoenzymatic Labeling of Aerolysin Enables the Identification of New Aerolysin Receptors
18. Site-Specific Chemoenzymatic Labeling of Aerolysin Enables the Identification of New Aerolysin Receptors
19. Epstein-Barr Virus Large Tegument Protein BPLF1 Contributes to Innate Immune Evasion through Interference with Toll-Like Receptor Signaling
20. Site-Specific Chemoenzymatic Labeling of Aerolysin Enables the Identification of New Aerolysin Receptors
21. Hyperactivating EZH2 to augment H3K27me3 levels in regulatory T cells enhances immune suppression by driving early effector differentiation.
22. Increased EZH2 function in regulatory T cells promotes their capacity to suppress autoimmunity by driving effector differentiation prior to activation.
23. Autoimmune disease-associated gene expression is reduced by BET-inhibition.
24. Inhibition of Super-Enhancer Activity in Autoinflammatory Site-Derived T Cells Reduces Disease-Associated Gene Expression.
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