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1. Prdm6 is essential for cardiovascular development in vivo.

2. Data from B-cell Expansion and Lymphomagenesis Induced by Chronic CD40 Signaling Is Strictly Dependent on CD19

3. Supplementary Figures 1 - 6 from B-cell Expansion and Lymphomagenesis Induced by Chronic CD40 Signaling Is Strictly Dependent on CD19

4. B-cell Expansion and Lymphomagenesis Induced by Chronic CD40 Signaling Is Strictly Dependent on CD19

5. MALT1 directs B cell receptor–induced canonical nuclear factor-κB signaling selectively to the c-Rel subunit

6. Bcl10/Malt1 Signaling Is Essential for TCR-Induced NF-κB Activation in Thymocytes but Dispensable for Positive or Negative Selection

7. Prdm6 is essential for cardiovascular development in vivo

8. Proteomic analysis of PAXgene-fixed tissues

9. A20 negatively regulates T cell receptor signaling to NF-kappaB by cleaving Malt1 ubiquitin chains

10. Malt1 ubiquitination triggers NF-κB signaling upon T-cell activation

11. Caspase-8 and c-FLIPL associate in lipid rafts with NF-kappaB adaptors during T cell activation

12. Bcl10 controls TCR- and FcgammaR-induced actin polymerization

13. Essential role for IkappaB kinase beta in remodeling Carma1-Bcl10-Malt1 complexes upon T cell activation

14. A model for PTCH1/Ptch1-associated tumors comprising mutational inactivation and gene silencing

15. Inhibition of MALT1 Protease Activity Is Selectively Toxic for Activated B CellÃ,–Like Diffuse Large B Cell Lymphoma Cells

16. Functional and Molecular Analysis of Maturation of Thymocytes in Bcl10 or Malt1 Deficient Mice

17. The fusion kinase ITK-SYK mimics a T cell receptor signal and drives oncogenesis in conditional mouse models of peripheral T cell lymphoma

18. Inhibition of MALT1 protease activity is selectively toxic for activated B cell?like diffuse large B cell lymphoma cells

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