Article in Genes & development, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors.
Lucas UngerMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.ORCID 0009-0003-1283-1813
Ulrik LarsenMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.
Thomas Aga LegøyMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.ORCID 0000-0001-7619-6220
Md Kaykobad HossainDepartment of Clinical Science, Faculty of Medicine, University of Bergen, 5020 Bergen, Norway.
June Helen GudmestadMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.
Amanda FriestadMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.
Shayla SharmineMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.
Pål Rasmus NjølstadMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.ORCID 0000-0003-0304-6728
Helge RæderMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.
Pedro Luis HerreraDepartment of Genetic Medicine and Development, Institute of Genetics and Genomics of Geneva (iGE3), Centre Facultaire du Diabète, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.ORCID 0000-0003-0771-9504
Luiza GhilaMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway.ORCID 0000-0001-7173-6312
Simona CheraMohn Research Center for Diabetes Precision Medicine, Department of Clinical Science, Faculty of Medicine, University of Bergen, 5009 Bergen, Norway; simona.chera@uib.no.ORCID 0000-0001-6310-3486
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
Regulatory circuits driving regional cell fate specification and lineage restriction decisions are not fully understood. The molecular mechanisms by which Hedgehog signaling controls lineage segregation in the posterior foregut remain unclear. Here, we employed bulk and single-cell transcriptomics, microscopy, physiology, and genetic cell tracing in differentiating human induced pluripotent stem cells and mouse transgenic models to uncover an essential autoregulatory loop between Hnf1a and Hedgehog signaling. Hnf1a abrogation initiates a domino effect leading to a drift in foregut cell specification toward duodenal cell identity instead of pancreatic fate. This was replicated in vivo in mice. We show that a common dominant negative
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 Socratic graph.
Defective HNF1A hinders GLI3 processing favoring duodenal versus pancreatic fate, thus leading to intestinal elongation in vivo. · full record | Socratic