532 results on '"Choi, Kang-Yell"'
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2. Inhibition of CXXC5 function rescues Alzheimer’s disease phenotypes by restoring Wnt/β-catenin signaling pathway
3. Metabolic improvement and liver regeneration by inhibiting CXXC5 function for non-alcoholic steatohepatitis treatment
4. Structural optimization of novel Ras modulator for treatment of Colorectal cancer by promoting β-catenin and Ras degradation
5. Differences in Proportion of N-acetyllactosamine and O-acetylated Sialic Acid Have No Significant Effect on the Pharmacokinetics and Biological Activity of Darbepoetin Alfa
6. Blockade of CXXC5-dishevelled interaction inhibits adipogenic differentiation, obesity, and insulin resistance in mice
7. Indirubin-3′-alkoxime derivatives for upregulation of Wnt signaling through dual inhibition of GSK-3β and the CXXC5-Dvl interaction
8. Deletion of phospholipase D1 decreases bone mass and increases fat mass via modulation of Runx2, β-catenin-osteoprotegerin, PPAR-γ and C/EBPα signaling axis
9. APC loss induces Warburg effect via increased PKM2 transcription in colorectal cancer
10. Destabilization of β-catenin and RAS by targeting the Wnt/β-catenin pathway as a potential treatment for triple-negative breast cancer
11. Transcutaneous implantation of valproic acid-encapsulated dissolving microneedles induces hair regrowth
12. Interaction of the Wnt/β-catenin and RAS-ERK pathways involving co-stabilization of both β-catenin and RAS plays important roles in the colorectal tumorigenesis
13. Indirubin-3′-oxime stimulates chondrocyte maturation and longitudinal bone growth via activation of the Wnt/β-catenin pathway
14. Pyruvate Kinase M2 Accelerates Cutaneous Wound Healing via Glycolysis and Wnt/β-Catenin Signaling
15. Targeting of CXXC5 by a Competing Peptide Stimulates Hair Regrowth and Wound-Induced Hair Neogenesis
16. 5-FU promotes stemness of colorectal cancer via p53-mediated WNT/β-catenin pathway activation
17. Small molecule-induced simultaneous destabilization of β-catenin and RAS is an effective molecular strategy to suppress stemness of colorectal cancer cells
18. WDR76 mediates obesity and hepatic steatosis via HRas destabilization
19. A Ras destabilizer KYA1797K overcomes the resistance of EGFR tyrosine kinase inhibitor in KRAS-mutated non-small cell lung cancer
20. WDR76 is a RAS binding protein that functions as a tumor suppressor via RAS degradation
21. A small molecule approach to degrade RAS with EGFR repression is a potential therapy for KRAS mutation-driven colorectal cancer resistance to cetuximab
22. Identification of Ras-degrading small molecules that inhibit the transformation of colorectal cancer cells independent of β-catenin signaling
23. Discovery of a small-molecule inhibitor of Dvl–CXXC5 interaction by computational approaches
24. Data from A Novel Role of Dipeptidyl Peptidase 9 in Epidermal Growth Factor Signaling
25. Supplementary Figures S1-S4 from A Novel Role of Dipeptidyl Peptidase 9 in Epidermal Growth Factor Signaling
26. Supplementary Figures 1-4, Supplementary Tables 1-2, Supplementary Figure Legends from Phospholipase D1 Inhibition Linked to Upregulation of ICAT Blocks Colorectal Cancer Growth Hyperactivated by Wnt/β-Catenin and PI3K/Akt Signaling
27. Supplementary Figure Legends from Phospholipase D1 Acts through Akt/TopBP1 and RB1 to Regulate the E2F1-Dependent Apoptotic Program in Cancer Cells
28. Supplementary Figures 1 through 11 from Phospholipase D1 Acts through Akt/TopBP1 and RB1 to Regulate the E2F1-Dependent Apoptotic Program in Cancer Cells
29. Supplementary Tables 1 through 4 from Phospholipase D1 Acts through Akt/TopBP1 and RB1 to Regulate the E2F1-Dependent Apoptotic Program in Cancer Cells
30. Supplementary Materials and Methods from Phospholipase D1 Inhibition Linked to Upregulation of ICAT Blocks Colorectal Cancer Growth Hyperactivated by Wnt/β-Catenin and PI3K/Akt Signaling
31. Supplementary Materials and Methods from Phospholipase D1 Acts through Akt/TopBP1 and RB1 to Regulate the E2F1-Dependent Apoptotic Program in Cancer Cells
32. Supplementary Figure 1 from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
33. Data from MEK1/2 Inhibitors AS703026 and AZD6244 May Be Potential Therapies for KRAS Mutated Colorectal Cancer That Is Resistant to EGFR Monoclonal Antibody Therapy
34. Data from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
35. Supplementary Methods, Figure Legends 1-6 from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
36. Supplementary Figure 2 from MEK1/2 Inhibitors AS703026 and AZD6244 May Be Potential Therapies for KRAS Mutated Colorectal Cancer That Is Resistant to EGFR Monoclonal Antibody Therapy
37. Supplementary Figure 6 from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
38. Supplementary Figure 3 from MEK1/2 Inhibitors AS703026 and AZD6244 May Be Potential Therapies for KRAS Mutated Colorectal Cancer That Is Resistant to EGFR Monoclonal Antibody Therapy
39. Supplementary Figure 4 from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
40. Supplementary Figure 2 from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
41. Supplementary Figure 5 from Phospholipase D1 Drives a Positive Feedback Loop to Reinforce the Wnt/β-Catenin/TCF Signaling Axis
42. Supplementary Figure 1 from MEK1/2 Inhibitors AS703026 and AZD6244 May Be Potential Therapies for KRAS Mutated Colorectal Cancer That Is Resistant to EGFR Monoclonal Antibody Therapy
43. Adhesive Hydrogel Patch‐Mediated Combination Drug Therapy Induces Regenerative Wound Healing through Reconstruction of Regenerative Microenvironment
44. Identification of small-molecule compounds targeting the dishevelled PDZ domain by virtual screening and binding studies
45. WDR76 degrades RAS and suppresses cancer stem cell activation in colorectal cancer
46. Lipid raft protein flotillin‐1 is important for the interaction between SOS1 and H‐Ras/K‐Ras, leading to Ras activation
47. CXXC5 Mediates DHT-Induced Androgenetic Alopecia via PGD2
48. β‐Catenin‐RAS interaction serves as a molecular switch for RAS degradation via GSK3β
49. Pyruvate Kinase M2 Promotes Hair Regeneration by Connecting Metabolic and Wnt/β-Catenin Signaling
50. Wnt/β-catenin signaling activator restores hair regeneration suppressed by diabetes mellitus
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