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E3 Ubiquitin Ligases in MASH‐Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities
ABSTRACT Metabolic dysfunction‐associated steatohepatitis (MASH) is a major cause of progressive liver fibrosis and can ultimately lead to cirrhosis and hepatocellular carcinoma (HCC). MASH‐associated liver fibrosis develops through a complex interplay among lipotoxic hepatocyte injury, oxidative and endoplasmic reticulum stress, inflammatory ...
Ah‐Reum Oh +8 more
wiley +1 more source
MDM2/X mediates reduced apoptosis in the plateau zokor: a mechanism of high-altitude adaptation. [PDF]
Zhang M +11 more
europepmc +1 more source
Targeting E3 ubiquitin ligases: Mechanistic breakthroughs and novel clinical translation pathways for tumor radioimmunotherapy. [PDF]
Yang Q +8 more
europepmc +1 more source
MDM2 Alters Cellular Iron Homeostasis by Promoting the Degradation of Proteins Involved in Iron Storage and Iron Export. [PDF]
Shi Y, Zhang J.
europepmc +1 more source
RING finger E3 ubiquitin ligases: novel therapeutic opportunities in melanoma. [PDF]
Zhang JF +7 more
europepmc +1 more source
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Current Pharmaceutical Design, 2012
The protein-protein interaction (PPI) between p53 and its negative regulator MDM2 comprises one of the most important and intensely studied PPI's involved in preventing the initiation of cancer. The interaction between p53 and MDM2 is conformation-based and is tightly regulated on multiple levels. Due to the Angstrom level structural insight there is a
Kareem, Khoury, Alex, Dömling
openaire +4 more sources
The protein-protein interaction (PPI) between p53 and its negative regulator MDM2 comprises one of the most important and intensely studied PPI's involved in preventing the initiation of cancer. The interaction between p53 and MDM2 is conformation-based and is tightly regulated on multiple levels. Due to the Angstrom level structural insight there is a
Kareem, Khoury, Alex, Dömling
openaire +4 more sources
MDM2-PROTAC versus MDM2 Inhibitors: Beyond p53 Reactivation
Cancer Discovery, 2023Summary: In this issue of Cancer Discovery, Adams and colleagues present the discovery of a potent PROTAC, MDM2 degrader, which activates wild-type p53 leading to cancer cell death. Importantly, in a number of in vitro and in vivo experiments, the authors show that the depletion of MDM2 by PROTAC kills p53 ...
Sylvain Peuget, Galina Selivanova
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