229 results on '"McCormick, Frank"'
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2. Abstract A018: A top-down proteomic assay to evaluate KRAS4B-compound engagement
3. Abstract B027: Bioluminescence resonance energy transfer (BRET) as a tool for assessing mutant KRAS-effector affinity and drug efficacy
4. Abstract PR01: Structural plasticity of KRAS oncogenic mutants – A case of misleading conclusions from GTP analogues
5. Abstract A033: KRAS codon 12 oncogenic mutations modulate protein conformation within the Switch II/Helix3 pocket
6. Abstract A028: An isogenic H/N/KRAS-less mouse embryonic fibroblast cell line panel derived from a size sorted diploid clonal parent
7. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
8. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
9. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
10. Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
11. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
12. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
13. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
14. Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
15. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
16. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
17. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis
18. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
19. Supplementary Table S5 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
20. Supplementary Table S4 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
21. Supplemental Figure and Table Legends from Development of siRNA Payloads to Target KRAS-Mutant Cancer
22. Supplementary Figure 3 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
23. Supplemental Table S2 from Development of siRNA Payloads to Target KRAS-Mutant Cancer
24. Supplementary Materials and Methods, Tables 1-2 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
25. Figure S4 from Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
26. Supplementary Methods, Table Legends, Figures 1 - 7 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
27. Supplementary Figure 6 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
28. Supplemental Figure and Table Legends from Development of siRNA Payloads to Target KRAS-Mutant Cancer
29. Supplemental References from Development of siRNA Payloads to Target KRAS-Mutant Cancer
30. Supplementary Methods, Table Legends, Figures 1 - 7 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
31. Figure S8 from Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
32. Data from Development of siRNA Payloads to Target KRAS-Mutant Cancer
33. Supplementary Figure 1 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
34. Supplementary Figure 4 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
35. Data from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
36. Supplementary Figure 2 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
37. Supplemental Table S2 from Development of siRNA Payloads to Target KRAS-Mutant Cancer
38. Data from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
39. Supplementary Figure 2 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
40. Supplementary Table S5 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
41. Figure S4 from Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
42. Supplementary Figure 1 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
43. Supplementary Figure 6 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
44. Supplemental Figure legends, Methods, Table S1 from Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
45. Figure S3 from Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
46. Supplemental Figure legends, Methods, Table S1 from Epithelial-to-Mesenchymal Transition Rewires the Molecular Path to PI3K-Dependent Proliferation
47. Supplementary Table S3 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
48. Supplemental Methods from Development of siRNA Payloads to Target KRAS-Mutant Cancer
49. Supplementary Table S2 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map
50. Supplementary Materials and Methods, Tables 1-2 from Oncogenic and Wild-type Ras Play Divergent Roles in the Regulation of Mitogen-Activated Protein Kinase Signaling
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