35 results on '"Delgado, Igotz"'
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2. THU-210 Dysfunctional activation of the DNA damage response is associated with MASLD progression through an E2F2-dependent mechanism
3. FRI-343-YI APAP induced liver damage is prevented by activation of PPARgamma and PPAR-alpha
4. OS-101-YI Remodelling of hepatocyte cholesterol metabolism mediates colorectal liver metastasis
5. TOP-229-YI The E2F2 target glycerophosphodiester phosphodiesterase domain containing 3 is involved in MASLD progression to HCC and related dyslipidemias
6. The E2F2-miR34a-5p axis is involved in the biliary metabolism dysregulation in NASH
7. Targeting the E2F/MCM axis in cholangiocarcinoma halts disease progression in experimental models by rewiring lipid metabolism
8. E2F2 deficiency protects from acetaminophen-induced hepatotoxicity while E2F1 is required to prevent the devastating effects
9. E2F2-promoted DNA damage in NASH worsens the metabolic scenario
10. Data from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
11. Supplementary Information from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
12. Supplementary Table 1 from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
13. Supplementary Data from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
14. Supplementary Table 2 from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
15. Supplementary Figures from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
16. Supplementary Table 3 from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
17. The uptake of extracellular lipids promotes cholangiocarcinoma progression
18. miR34a-5p is a target of E2F2 transcription factor in MAFLD-related HCC
19. The DNA damage response is involved in the metabolic dysregulation of MAFLD patients via inefficient fatty acid oxidation
20. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids
21. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids
22. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids
23. E2F1 and E2F2-mediated repression of CPT2 establishes a lipid-rich tumor-promoting environment
24. E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
25. WED-408 - E2F2-promoted DNA damage in NASH worsens the metabolic scenario
26. WED-404 - The E2F2-miR34a-5p axis is involved in the biliary metabolism dysregulation in NASH
27. SAT-215 - Targeting the E2F/MCM axis in cholangiocarcinoma halts disease progression in experimental models by rewiring lipid metabolism
28. FRI-395 - E2F2 deficiency protects from acetaminophen-induced hepatotoxicity while E2F1 is required to prevent the devastating effects
29. Hedgehog Signaling Is Critical for Normal Liver Regeneration After Partial Hepatectomy in Mice
30. PS-008-E2F2 mediated repression of fatty acid B-oxidation is mitigated through CREB1 in progressive non-alcoholic fatty liver disease
31. PTEN recruitment controls synaptic and cognitive function in Alzheimer's models
32. The E2F2 Transcription Factor Sustains Hepatic Glycerophospholipid Homeostasis in Mice
33. p53 Serves as a Host Antiviral Factor That Enhances Innate and Adaptive Immune Responses to Influenza A Virus
34. A role for transcription factor E2F2 in hepatocyte proliferation and timely liver regeneration
35. A role for transcription factor E2F2 in hepatocyte proliferation and timely liver regeneration.
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