253 results on '"Pandita, Tej K."'
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2. Cyclin-dependent kinases in cancer: Role, regulation, and therapeutic targeting
3. A prismatic view of the epigenetic-metabolic regulatory axis in breast cancer therapy resistance
4. Role of the Histone Acetyl Transferase MOF and the Histone Deacetylase Sirtuins in Regulation of H4K16ac During DNA Damage Repair and Metabolic Programming: Implications in Cancer and Aging
5. Correction: The Role of the Mammalian DNA End-processing Enzyme Polynucleotide Kinase 3’-Phosphatase in Spinocerebellar Ataxia Type 3 Pathogenesis
6. Ubiquitination and deubiquitination: Implications on cancer therapy
7. Ubiquitin specific peptidase 37 and PCNA interaction promotes osteosarcoma pathogenesis by modulating replication fork progression
8. Abstract 335: Ubiquitin Specific Peptidase 37promotes Osteosarcoma oncogenesis by interacting with PCNA and impacting constitutive replication fork movement.
9. Supplementary Methods from The Proteasome Activator PA200 Regulates Tumor Cell Responsiveness to Glutamine and Resistance to Ionizing Radiation
10. Supplementary Figures 1-2 from The Proteasome Activator PA200 Regulates Tumor Cell Responsiveness to Glutamine and Resistance to Ionizing Radiation
11. Supplementary Methods from The Proteasome Activator PA200 Regulates Tumor Cell Responsiveness to Glutamine and Resistance to Ionizing Radiation
12. Supplementary Figures 1-2 from The Proteasome Activator PA200 Regulates Tumor Cell Responsiveness to Glutamine and Resistance to Ionizing Radiation
13. Supplemental Figures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
14. Supplementary Table 1-3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
15. Data from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
16. Supplemental table S1 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
17. Supplemental table S1 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
18. Figure S5 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
19. Figure S4 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
20. Extended supplementary procedures from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
21. Figure S5 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
22. Supplemental experimental Procedures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
23. Supplemental Table S2 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
24. Related Article from Does PTEN Loss Impair DNA Double-Strand Break Repair by Homologous Recombination?
25. Supplemental Figures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
26. Figure S3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
27. Figure S2 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
28. Supplemental experimental Procedures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
29. Data from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
30. Figure S1 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
31. Figure S4 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
32. Extended supplementary procedures from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
33. Supplementary Table 1-3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
34. Figure S1 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
35. Data from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
36. Data from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
37. Supplemental Table S2 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
38. Figure S2 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition
39. Related Article from Does PTEN Loss Impair DNA Double-Strand Break Repair by Homologous Recombination?
40. Supplementary Table 2 from Epigenetic Inactivation of the Potential Tumor Suppressor Gene FOXF1 in Breast Cancer
41. Supplementary Figures 1-5 from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs
42. Data from Epigenetic Inactivation of the Potential Tumor Suppressor Gene FOXF1 in Breast Cancer
43. Data from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs
44. Data from Negative Regulation of AKT Activation by BRCA1
45. Supplementary Methods from Epigenetic Inactivation of the Potential Tumor Suppressor Gene FOXF1 in Breast Cancer
46. Supplementary Figure 1, Table 1 from Inhibition of Telomerase Activity Enhances Hyperthermia-Mediated Radiosensitization
47. Data from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs
48. Data from Epigenetic Inactivation of the Potential Tumor Suppressor Gene FOXF1 in Breast Cancer
49. Data from Inhibition of Telomerase Activity Enhances Hyperthermia-Mediated Radiosensitization
50. Supplementary Table 2 from Epigenetic Inactivation of the Potential Tumor Suppressor Gene FOXF1 in Breast Cancer
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