19 results on '"Aurrekoetxea, Igor"'
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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. S-Adenosylmethionine increases circulating very-low density lipoprotein clearance in non-alcoholic fatty liver disease
11. The uptake of extracellular lipids promotes cholangiocarcinoma progression
12. miR34a-5p is a target of E2F2 transcription factor in MAFLD-related HCC
13. Methionine adenosyltransferase 1a antisense oligonucleotides induce the fibroblast growth factor 21-driven recovery from obesity and associated hepatoesteatosis
14. The DNA damage response is involved in the metabolic dysregulation of MAFLD patients via inefficient fatty acid oxidation
15. WED-408 - E2F2-promoted DNA damage in NASH worsens the metabolic scenario
16. WED-404 - The E2F2-miR34a-5p axis is involved in the biliary metabolism dysregulation in NASH
17. SAT-215 - Targeting the E2F/MCM axis in cholangiocarcinoma halts disease progression in experimental models by rewiring lipid metabolism
18. FRI-395 - E2F2 deficiency protects from acetaminophen-induced hepatotoxicity while E2F1 is required to prevent the devastating effects
19. PS-008-E2F2 mediated repression of fatty acid B-oxidation is mitigated through CREB1 in progressive non-alcoholic fatty liver disease
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