ArticleThe FEBS journal2026
Disruption of iron metabolism resulting from Dmt1/Slc11a2 deficiency compromises Notch protein degradation and transcriptional activation.
Article in The FEBS journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Lysosomal metabolism in pancreatic cancer and its crosstalk with host physiology.Genes & development · 2026Review
- SLC11A2 withholds divalent metals fromProceedings of the National Academy of Sciences of the United States of America · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Notch receptor activation requires γ-secretase-mediated release of Notch intracellular domain 1 (NICD1) to regulate gene transcription. Here, we identify the proton-driven solute carrier 11a2 (Slc11a2) or divalent metal transport protein Dmt1 as an inhibitor of Notch signaling via regulating iron homeostasis and lysosomal integrity. Dmt1 loss reduces ferritin levels and increases labile Fe
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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.