Evidence map›Paper›PMID 31186352›Full record

ArticleThe Journal of biological chemistry2019

The nuclear pore proteins Nup88/214 and T-cell acute lymphatic leukemia-associated NUP214 fusion proteins regulate Notch signaling.

Bastian Kindermann, Christina Valkova, Andreas Krämer, Birgit Perner, Christian Engelmann, Laura Behrendt, Daniel Kritsch, Berit Jungnickel, Ralph H Kehlenbach, Franz Oswald and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 44% of its field
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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Dysregulated genes in HIGK-treatedMolecular biology research communications · 2025
    Article
  3. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  4. Review
4 · The record

Corrections and comments

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 at 4 institutions in 1 country.

Bastian KindermannLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Christina ValkovaLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Andreas KrämerLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Birgit PernerLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Christian EngelmannLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Laura BehrendtLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Daniel KritschInstitut für Biochemie und Biophysik, Friedrich Schiller Universität Jena, 07745 Jena, Germany.
Berit JungnickelInstitut für Biochemie und Biophysik, Friedrich Schiller Universität Jena, 07745 Jena, Germany.
Ralph H KehlenbachDepartment of Molecular Biology, Universitätsmedizin Göttingen, 37073 Göttingen, Germany.ORCID 0000-0003-4920-9916
Franz OswaldUniversitätsklinikum Ulm, Zentrum für Innere Medizin, Abteilung für Innere Medizin I, 89081 Ulm, Germany.
Christoph EnglertLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany.
Christoph KaetherLeibniz Institut für Alternsforschung-Fritz Lipmann Institut, 07745 Jena, Germany ckaether@fli-leibniz.de.ORCID 0000-0002-6874-2276
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEFriedrich Schiller University Jena · DEUniversitätsmedizin Göttingen · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Notch receptor is a key mediator of developmental programs and cell-fate decisions. Imbalanced Notch signaling leads to developmental disorders and cancer. To fully characterize the Notch signaling pathway and exploit it in novel therapeutic interventions, a comprehensive view on the regulation and requirements of Notch signaling is needed. Notch is regulated at different levels, ranging from ligand binding, stability to endocytosis. Using an array of different techniques, including reporter gene assays, immunocytochemistry, and ChIP-qPCR we show here, to the best of our knowledge for the first time, regulation of Notch signaling at the level of the nuclear pore. We found that the nuclear pore protein Nup214 (nucleoporin 214) and its interaction partner Nup88 negatively regulate Notch signaling

Indexed as

Signal TransductionActive Transport, Cell NucleusAnimalsCell Line, TumorHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinMorpholinosNuclear Pore Complex ProteinsPrecursor T-Cell Lymphoblastic Leukemia-LymphomaReceptors, NotchRecombinant Fusion ProteinsRNA InterferenceRNA, Small InterferingTranscription Factor HES-1ZebrafishZebrafish ProteinsHES1 protein, humanImmunoglobulin J Recombination Signal Sequence-Binding ProteinMorpholinosNuclear Pore Complex ProteinsNUP214 protein, humanNUP88 protein, humanRBPJ protein, humanReceptors, NotchRecombinant Fusion ProteinsRNA, Small InterferingTranscription Factor HES-1Zebrafish Proteinscancercell compartmentalizationcell signalinggene regulationleukemiaNotch pathwaynuclear porenuclear transportnucleoporin 214 (Nup214)nucleoporin 88 (Nup88)recombination signal–binding protein for immunoglobulin kappa J region (RBP-J)T-cell acute lymphatic leukemia (T-ALL)

Identifiers

PMID31186352
PMCPMC6682737
OpenAlexW2966923827

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.