473 results on '"Delia, Domenico"'
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2. Parkinson’s disease patients display a DNA damage signature in blood that is predictive of disease progression
3. Immune-tolerance to human iPS-derived neural progenitors xenografted into the immature cerebellum is overridden by species-specific differences in differentiation timing
4. Chapter 7 - Clinical and molecular findings in Ataxia–Telangiectasia
5. Detection of ATM Gene Mutation in Human Glioma Cell Line M059J by a Rapid Frameshift/Stop Codon Assay in Yeast
6. Lemur tyrosine kinase 2 (LMTK2) is a determinant of cell sensitivity to apoptosis by regulating the levels of the BCL2 family members
7. Poly (ADP-ribose) polymerase inhibitors selectively induce cytotoxicity in TCF3-HLF–positive leukemic cells
8. DNA damage and transcriptional regulation in iPSC-derived neurons from Ataxia Telangiectasia patients
9. The Tumor-Suppressor Gene FHIT Is Involved in the Regulation of Apoptosis and in Cell Cycle Control
10. The Antisense bcl-2-igH Transcript is an Optimal Target for Synthetic Oligonucleotides
11. Supplementary Movie 1 from TRAP1 Regulates Proliferation, Mitochondrial Function, and Has Prognostic Significance in NSCLC
12. Supplementary Movie 2 from TRAP1 Regulates Proliferation, Mitochondrial Function, and Has Prognostic Significance in NSCLC
13. Data from TRAP1 Regulates Proliferation, Mitochondrial Function, and Has Prognostic Significance in NSCLC
14. Supplementary Figures S1-S6 from Tumor-Initiating Cells of HER2-Positive Carcinoma Cell Lines Express the Highest Oncoprotein Levels and Are Sensitive to Trastuzumab
15. Translation on this Article from Tumor-Initiating Cells of HER2-Positive Carcinoma Cell Lines Express the Highest Oncoprotein Levels and Are Sensitive to Trastuzumab
16. Supplementary Figure 7 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
17. Supplementary Figure 6 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
18. Supplementary Figure 8 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
19. Supplementary Table 1 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
20. Supplementary Methods and Figure Legends from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
21. Supplementary Figure 9 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
22. Supplementary Figure 3 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
23. Supplementary Figure 2 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
24. Supplementary Figure 1 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
25. Supplementary Figure 2 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
26. Supplementary Table 4 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
27. Supplementary Figure 4 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
28. Supplementary Figure 4 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
29. Data from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
30. Data from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
31. Supplementary Figure 3 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
32. Supplementary Table 1 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
33. Supplementary Figure 5 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
34. Supplementary Table 2 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
35. Supplementary Figure 5 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
36. Supplementary Table 3 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
37. Supplementary Figure 1 from TLR9 Agonists Oppositely Modulate DNA Repair Genes in Tumor versus Immune Cells and Enhance Chemotherapy Effects
38. Supplementary Figure 6 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
39. Supplementary Table 2 from Chk2 Phosphorylation of Survivin-ΔEx3 Contributes to a DNA Damage–Sensing Checkpoint in Cancer
40. Dissociation between cell cycle arrest and apoptosis can occur in Li-Fraumeni cells heterozygous for p53 gene mutations
41. The DNA damage response pathway in normal hematopoiesis and malignancies
42. List of Contributors
43. MiR-16 regulates the pro-tumorigenic potential of lung fibroblasts through the inhibition of HGF production in an FGFR-1- and MEK1-dependent manner
44. Pressure Overload Activates DNA-Damage Response in Cardiac Stromal Cells: A Novel Mechanism Behind Heart Failure With Preserved Ejection Fraction?
45. Single-agent Smac-mimetic compounds induce apoptosis in B chronic lymphocytic leukaemia (B-CLL)
46. Dimeric Smac mimetics/IAP inhibitors as in vivo-active pro-apoptotic agents. Part II: Structural and biological characterization
47. Highly Tumorigenic Lung Cancer CD133⁺ Cells Display Stem-Like Features and Are Spared by Cisplatin Treatment
48. Hemopoietic Cell Differentiation and Death By Retinoids
49. Integrins and Homing Receptors in Cutaneous Lymphomas
50. Rational design, synthesis and characterization of potent, non-peptidic Smac mimics/XIAP inhibitors as proapoptotic agents for cancer therapy
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