In one paragraphArticle in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
13 authors.
Mirjam Elisabeth HoenessDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
Franziska ZellDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0009-0003-1984-6292 Titiksha BasuDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
Katharina GellrichDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
Albert GründerDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
Jana SchulzeDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0009-0006-1682-4487 Anja MüllerDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0009-0009-6100-0788 Philipp EbleDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0009-0007-2915-3966 Christoph KoellererDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0009-0006-9919-7852 Anne Marie StaehleDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0009-0006-7977-0121 Sarolta Bojtine KovacsDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
Heike L PahlDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0003-2857-2396 Hans Felix StaehleDivision of Molecular Hematology, Department of Medicine I, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0001-5082-0646 Funding
Deutsche Forschungsgemeinschaft Pa 611/11-1Deutsche Forschungsgemeinschaft Pa 611/5-3Else Kröner-Fresenius-Stiftung 2016_Kolleg_15Else Kröner-Fresenius-Stiftung 2021_EKEA.122
6 · The paper itselfAbstract
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic disorders characterized by the abnormal proliferation of myeloid cells. In addition to the main driver mutations in JAK2, MPL, and CALR, the transcription factor nuclear factor erythroid 2 (NFE2) has emerged as a key contributor to MPN pathophysiology. NFE2 expression is elevated in the majority of MPN patients, and augmented NFE2 activity in hematopoietic stem cells is sufficient to induce an MPN phenotype with spontaneous leukemic transformation in murine models. Moreover, NFE2 mutations, found in a subset of MPN patients, augment NFE2 activity and are associated with a markedly increased risk of progression to acute myeloid leukemia (AML). However, the molecular mechanism by which NFE2 mutations cause leukemogenesis is not understood. Here, we demonstrate that the E3 ubiquitin ligase ITCH mediates proteasomal degradation of wild-type (wt) NFE2 in HEK-293T cells. A gain-of-function truncation mutant, NFE2-226aa, retains the capacity to interact with ITCH but is no longer degraded. Rather, NFE2-226aa protects wt NFE2 from ITCH-dependent degradation, resulting in enhanced NFE2 activity.
Indexed as
MutationMyeloproliferative DisordersNF-E2 Transcription Factor, p45 SubunitUbiquitin-Protein LigasesAnimalsHEK293 CellsHumansMiceProteolysisRepressor ProteinsITCH protein, humanNFE2 protein, humanNF-E2 Transcription Factor, p45 SubunitRepressor ProteinsUbiquitin-Protein LigasesITCHMPNNFE2
Identifiers
PMID41465537
PMCPMC12733253
What OpenQuestion holds
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LicenceCC BY
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