48 results on '"Rabellino, Andrea"'
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2. Direct stimulation of ERBB2 highlights a novel cytostatic signaling pathway driven by the receptor Thr701 phosphorylation
3. PIAS1 Promotes Lymphomagenesis through MYC Upregulation
4. Roles of Ubiquitination and SUMOylation in the Regulation of Angiogenesis
5. Data from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
6. Supplementary Figure 4 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
7. Supplementary Figure 2 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
8. Supplementary Figure 3 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
9. Supplementary Methods, Figure Legends from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
10. Supplementary Figure 5 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
11. Supplementary Figure 1 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
12. Supplementary Table 1 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
13. Supplementary Figure 6 from Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
14. Supplementary Methods, Figure Legends 1-6 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
15. Supplementary Figure 6 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
16. Supplementary Table 1 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
17. Supplementary Figure 1 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
18. Data from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
19. Supplementary Figure 5 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
20. Supplementary Figure 3 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
21. Supplementary Figure 1 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
22. Supplementary Figure 5 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
23. Supplementary Figure 4 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
24. Supplementary Figure 2 from The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
25. Supplementary Table 1 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
26. Supplementary Table 2 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
27. Supplementary Tables 1-2, Figures 1-5 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
28. Supplementary Figure 4 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
29. Data from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
30. Supplementary Figure 3 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
31. Supplementary Figure 2 from Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
32. Ligation of the BT3 molecules, members of the B7 family, enhance the proinflammatory responses of human monocytes and monocyte-derived dendritic cells
33. Translation‐dependent mechanisms lead to PML upregulation and mediate oncogenic K‐RAS‐induced cellular senescence
34. The implication of the SUMOylation pathway in breast cancer pathogenesis and treatment
35. Roles of Ubiquitination and SUMOylation in the Regulation of Angiogenesis
36. RAD51 paralogs promote genomic integrity and chemoresistance in cancer by facilitating homologous recombination
37. The Role of PIAS SUMO E3-Ligases in Cancer
38. A comprehensive analysis of Trastuzumab-induced signaling suggests the role of HER2 in several cell processes and highlights alternative targets for HER2- positive breast cancer therapy
39. Nullifying the CDKN2AB Locus Promotes Mutant K-ras Lung Tumorigenesis
40. The SUMO Ligase PIAS1 Promotes the Progression and Survival of Solid Tumors of Different Histopathological Origins
41. PML Degradation: Multiple Ways to Eliminate PML
42. The SUMO E3-ligase PIAS1 Regulates the Tumor Suppressor PML and Its Oncogenic Counterpart PML-RARA
43. Dual Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Blockade Is an Effective Radiosensitizing Strategy for the Treatment of Non–Small Cell Lung Cancer Harboring K-RAS Mutations
44. Relationships between EGFR Signaling–competent and Endocytosis-competent Membrane Microdomains
45. Author Correction: Direct stimulation of ERBB2 highlights a novel cytostatic signaling pathway driven by the receptor Thr701 phosphorylation.
46. Direct stimulation of ERBB2 highlights a novel cytostatic signaling pathway driven by the receptor Thr701 phosphorylation.
47. Translation-dependent mechanisms lead to PML upregulation and mediate oncogenic K-RAS-induced cellular senescence
48. ERBB2 activation leads to an anti-oncogenic signalling.
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