ArticleInternational journal of molecular sciences2022
EAPB0503, an Imidazoquinoxaline Derivative Modulates SENP3/ARF Mediated SUMOylation, and Induces NPM1c Degradation in NPM1 Mutant AML.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- The Novel Imiqualine EAPB02303 Is a Potent Drug for Treating Acute Myeloid Leukemia.Biomolecules · 2025Article
- Influence of Nucleophosmin (Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Article
- Synthesis and evaluation of imidazo[1,2-a]quinoxaline derivatives as potential antifungal agents against phytopathogenic fungi.Molecular diversity · 2024Article
- Uncovering the Molecular Pathways Implicated in the Anti-Cancer Activity of the Imidazoquinoxaline Derivative EAPB02303 Using aInternational journal of molecular sciences · 2024Article
- Could Targeting NPM1c+ Misfolding Be a Promising Strategy for Combating Acute Myeloid Leukemia?International journal of molecular sciences · 2024Review
- [1,2,4]triazolo[4,3-Molecules (Basel, Switzerland) · 2023Article
- Identification of Potential Antitubulin Agents with Anticancer Assets from a Series of Imidazo[1,2-Molecules (Basel, Switzerland) · 2023Article
- Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Nucleophosmin-1 (NPM1) is a pleiotropic protein involved in numerous cellular processes. NPM1 shuttles between the nucleus and the cytoplasm, but exhibits a predominant nucleolar localization, where its fate and functions are exquisitely controlled by dynamic post-translational modifications (PTM). Sentrin/SUMO Specific Peptidase 3 (SENP3) and ARF are two nucleolar proteins involved in NPM1 PTMs. SENP3 antagonizes ARF-mediated NPM1 SUMOylation, to promote ribosomal biogenesis. In Acute Myeloid Leukemia (AML), NPM1 is frequently mutated, and exhibits an aberrant cytoplasmic localization (NPM1c). NPM1c mutations define a separate AML entity with good prognosis in some AML patients, rendering NPM1c as a potential therapeutic target. SENP3-mediated NPM1 de-SUMOylation induces resistance to therapy in NPM1c AML. Here, we demonstrate that the imidazoquinoxaline EAPB0503 prolongs the survival and results in selective reduction in the leukemia burden of NPM1c AML xenograft mice. Indeed, EAPB0503 selectively downregulates HDM2 expression and activates the
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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.