ArticleiScience2026
Inhibiting MDM2 enhances RIPK3-mediated necroptosis and synergizes with immune checkpoint blockade therapy.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis is a form of programmed cell death that promotes tumor immunogenicity. To identify druggable regulators of necroptosis, we performed a small-molecule inhibitor screen and identified mouse double minute 2 (MDM2) as a suppressor of tumor necrosis factor α (TNF-α)-induced necroptosis. Genetic deletion or pharmacologic inhibition of MDM2 markedly enhanced necroptosis in a receptor-interacting protein kinase 1 (RIPK1)-dependent and p53-independent manner. Mechanistically, MDM2 interacted with RIPK3 and promoted its proteasome-mediated degradation, thereby limiting RIPK3 abundance and restraining pathway activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.