425 results on '"Rauh, Daniel"'
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2. Persister state-directed transitioning and vulnerability in melanoma
3. Functional noninvasive detection of glycolytic pancreatic ductal adenocarcinoma
4. Chemische Biologie
5. Inhibition of Tumor VEGFR2 Induces Serine 897 EphA2-Dependent Tumor Cell Invasion and Metastasis in NSCLC
6. Targeting KRAS Diversity: Covalent Modulation of G12X and Beyond in Cancer Therapy
7. Akt Inhibitor Advancements: From Capivasertib Approval to Covalent-Allosteric Promises
8. 11th German Conference on Chemoinformatics (GCC 2015) : Fulda, Germany. 8-10 November 2015.
9. Cellular model system to dissect the isoform-selectivity of Akt inhibitors
10. Correction: A high-throughput effector screen identifies a novel small molecule scaffold for inhibition of ten-eleven translocation dioxygenase 2
11. Reply to Y. Xia et al.
12. 2-Azo-, 2-diazocine-thiazols and 2-azo-imidazoles as photoswitchable kinase inhibitors: limitations and pitfalls of the photoswitchable inhibitor approach
13. Systematic Kinase Inhibitor Profiling Identifies CDK9 as a Synthetic Lethal Target in NUT Midline Carcinoma
14. Fragtory: Pharmacophore-Focused Design, Synthesis, and Evaluation of an sp3-Enriched Fragment Library
15. A novel scaffold for EGFR inhibition: Introducing N-(3-(3-phenylureido)quinoxalin-6-yl) acrylamide derivatives
16. Addressing the Osimertinib Resistance Mutation EGFR-L858R/C797S with Reversible Aminopyrimidines
17. Abstract 3887: ATP-binding pocket substitutions as secondary or tertiary in-cis mutations are major on-target ripretinib resistance mechanisms in gastrointestinal stromal tumor
18. Supplementary Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain
19. Data from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
20. Data from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified FGFR1 in Lung Cancer
21. Interview with Dr. Meyerson from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
22. Supplementary Methods and Legends from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified FGFR1 in Lung Cancer
23. Supplementary Figure Legends 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
24. Supplementary Figures 1-7 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
25. Supplementary Table 1 from Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer
26. Data from Resistance to Avapritinib in PDGFRA-Driven GIST Is Caused by Secondary Mutations in the PDGFRA Kinase Domain
27. Supplementary Figures S1-S14 from Cell-Autonomous and Non–Cell-Autonomous Mechanisms of Transformation by Amplified FGFR1 in Lung Cancer
28. Glucocorticoid activation by HSD11B1 limits T cell-driven interferon signaling and response to PD-1 blockade in melanoma
29. Data from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors
30. Supplementary Figures 1-9 from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors
31. Supplementary Figure Legends 1-9 from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors
32. Supplementary Table 1 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
33. Supplementary Figure 2 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
34. Supplementary Methods, Figure Legends 1-3 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
35. Supplementary Figure 3 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
36. Supplementary Table 2 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
37. Supplementary Figure 4 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
38. Supplementary Figure 1 from Chemogenomic Profiling Provides Insights into the Limited Activity of Irreversible EGFR Inhibitors in Tumor Cells Expressing the T790M EGFR Resistance Mutation
39. Targeting oncogenic KRasG13C with nucleotide-based covalent inhibitors
40. Insights into the Conformational Plasticity of the Protein Kinase Akt1 by Multi‐Lateral Dipolar Spectroscopy
41. A Synergistic Interaction between Chk1- and MK2 Inhibitors in KRAS-Mutant Cancer
42. Structure-based design and synthesis of covalent-reversible inhibitors to overcome drug resistance in EGFR
43. Additional file 1 of Functional noninvasive detection of glycolytic pancreatic ductal adenocarcinoma
44. Additional file 2 of Functional noninvasive detection of glycolytic pancreatic ductal adenocarcinoma
45. Towards Clinical AKT Inhibition in Glioblastoma
46. Overcoming EGFRG724S-mediated osimertinib resistance through unique binding characteristics of second-generation EGFR inhibitors
47. Fragtory: Pharmacophore-Focused Design, Synthesis, and Evaluation of an sp3‑Enriched Fragment Library.
48. Optimization of Covalent MKK7 Inhibitors via Crude Nanomole-Scale Libraries
49. Targeting oncogenic KRasG13C with nucleotide-based covalent inhibitors
50. Design and synthesis of Nrf2-derived hydrocarbon stapled peptides for the disruption of protein-DNA-interactions
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