Article in Genes & development, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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
20 authors.
Kazuko Miyazaki *Laboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.ORCID 0000-0001-9754-698X
Kenta Horie *Laboratory for Immune Homeostasis, RIKEN Center for Integrative Medical Sciences, Kanagawa 230-0045, Japan.ORCID 0000-0003-4175-1014
Hitomi Watanabe *Laboratory of Integrative Biological Sciences, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Reiko Hidaka *Laboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Rinako HayashiLaboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Norihito HayatsuLaboratory for Comprehensive Genomic Analysis, RIKEN Center for Integrative Medical Sciences, Kanagawa 230-0045, Japan.
Kentaro FujiwaraLaboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Rei KuwataLaboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Takuya UehataDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0003-3517-2198
Yotaro OchiDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0001-8472-6164
Makoto TakenakaLaboratory of Integrative Biological Sciences, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Risa Karakida KawaguchiCenter for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.ORCID 0000-0003-1764-5721
Koichi IkutaLaboratory of Immune Regulation, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.ORCID 0000-0003-1319-1021
Osamu TakeuchiDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0002-1260-6232
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0002-7778-5374
Katsuto HozumiDepartment of Immunology, Tokai University School of Medicine, Kanagawa 259-1193, Japan.ORCID 0000-0002-7685-6927
Georg A HolländerDepartment of Pediatrics, Institute of Developmental and Regenerative Medicine, University of Oxford, Oxford OX3 7TY, United Kingdom.ORCID 0000-0002-8790-0874
Gen KondohLaboratory of Integrative Biological Sciences, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.ORCID 0000-0002-2564-0149
Taishin AkiyamaLaboratory for Immune Homeostasis, RIKEN Center for Integrative Medical Sciences, Kanagawa 230-0045, Japan.ORCID 0000-0002-0341-6154
Masaki MiyazakiLaboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan; mmiyazaki@infront.kyoto-u.ac.jp.ORCID 0000-0002-9543-624X
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
External signals from the thymic microenvironment and the activities of lineage-specific transcription factors (TFs) instruct T-cell versus innate lymphoid cell (ILC) fates. However, mechanistic insights into how factors such as Notch1-Delta-like-4 (Dll4) signaling and E-protein TFs collaborate to establish T-cell identity remain rudimentary. Using multiple in vivo approaches and single-cell multiome analysis, we identified a feedback amplifier circuit that specifies fetal and adult T-cell fates. In early T progenitors (ETPs) in the fetal thymus, Notch signaling minimally lowered E-protein antagonist
Indexed as
Basic Helix-Loop-Helix ProteinsCell LineageFeedback, PhysiologicalImmunity, InnateLymphocytesReceptors, NotchThymus GlandT-LymphocytesAnimalsCell DifferentiationGene Expression Regulation, DevelopmentalInhibitor of Differentiation Protein 2MiceMice, Inbred C57BLSignal TransductionBasic Helix-Loop-Helix ProteinsIdb2 protein, mouseInhibitor of Differentiation Protein 2Receptors, Notchenhancer landscapeE-protein E2Alymphoid lineagesNotch signalingT-cell lineage commitmentthymic ontogeny
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.
A feedback amplifier circuit with Notch and E2A orchestrates T-cell fate and suppresses the innate lymphoid cell lineages during thymic ontogeny. · full record | Socratic