34 results on '"Aurrekoetxea, Igor"'
Search Results
2. In Vivo Hepatic Triglyceride Secretion Rate in Antisense Oligonucleotide (ASO)-Treated Mice
3. FRI-472-YI Mitochondrial metabolism is disrupted by ciprofloxacin preventing cholangiocarcinoma cell proliferation
4. THU-210 Dysfunctional activation of the DNA damage response is associated with MASLD progression through an E2F2-dependent mechanism
5. FRI-343-YI APAP induced liver damage is prevented by activation of PPARgamma and PPAR-alpha
6. OS-101-YI Remodelling of hepatocyte cholesterol metabolism mediates colorectal liver metastasis
7. TOP-229-YI The E2F2 target glycerophosphodiester phosphodiesterase domain containing 3 is involved in MASLD progression to HCC and related dyslipidemias
8. Methionine adenosyltransferase 1a antisense oligonucleotides activate the liver-brown adipose tissue axis preventing obesity and associated hepatosteatosis
9. The E2F2-miR34a-5p axis is involved in the biliary metabolism dysregulation in NASH
10. Targeting the E2F/MCM axis in cholangiocarcinoma halts disease progression in experimental models by rewiring lipid metabolism
11. E2F2 deficiency protects from acetaminophen-induced hepatotoxicity while E2F1 is required to prevent the devastating effects
12. E2F2-promoted DNA damage in NASH worsens the metabolic scenario
13. Data from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
14. Supplementary Information from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
15. Supplementary Table 1 from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
16. Supplementary Data from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
17. Supplementary Table 2 from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
18. Supplementary Figures from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
19. Supplementary Table 3 from E2F1 and E2F2-Mediated Repression of CPT2 Establishes a Lipid-Rich Tumor-Promoting Environment
20. Targeting E2F Sensitizes Prostate Cancer Cells to Drug-Induced Replication Stress by Promoting Unscheduled CDK1 Activity
21. The uptake of extracellular lipids promotes cholangiocarcinoma progression
22. miR34a-5p is a target of E2F2 transcription factor in MAFLD-related HCC
23. Methionine adenosyltransferase 1a antisense oligonucleotides induce the fibroblast growth factor 21-driven recovery from obesity and associated hepatoesteatosis
24. The DNA damage response is involved in the metabolic dysregulation of MAFLD patients via inefficient fatty acid oxidation
25. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids
26. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids
27. Cholangiocarcinoma progression depends on the uptake and metabolization of extracellular lipids
28. WED-408 - E2F2-promoted DNA damage in NASH worsens the metabolic scenario
29. WED-404 - The E2F2-miR34a-5p axis is involved in the biliary metabolism dysregulation in NASH
30. SAT-215 - Targeting the E2F/MCM axis in cholangiocarcinoma halts disease progression in experimental models by rewiring lipid metabolism
31. FRI-395 - E2F2 deficiency protects from acetaminophen-induced hepatotoxicity while E2F1 is required to prevent the devastating effects
32. Neddylation inhibition prevents acetaminophen-induced liver damage by enhancing the anabolic cardiolipin pathway
33. In Vivo Hepatic Triglyceride Secretion Rate in Antisense Oligonucleotide (ASO)-Treated Mice.
34. In Vivo Tissue Lipid Uptake in Antisense Oligonucleotide (ASO)-Treated Mice.
Catalog
Books, media, physical & digital resources
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.