ArticleMolecular biology of the cell2010
Nup98-homeodomain fusions interact with endogenous Nup98 during interphase and localize to kinetochores and chromosome arms during mitosis.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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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.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Condensates in fusion oncoprotein-driven leukemia: new biology and therapeutic opportunities.Trends in cancer · 2026Review
- Article
- Phase Separation Mediates NUP98 Fusion Oncoprotein Leukemic Transformation.Cancer discovery · 2022Article
- Article
- A genetic screen in Drosophila uncovers the multifaceted properties of the NUP98-HOXA9 oncogene.PLoS genetics · 2021Article
- Ribonucleic Acid Export 1 Is a Kinetochore-Associated Protein That Participates in Chromosome Alignment in Mouse Oocytes.International journal of molecular sciences · 2021Article
- Biomolecular condensation of NUP98 fusion proteins drives leukemogenic gene expression.Nature structural & molecular biology · 2021Article
- Article
- Formation of Nup98-containing nuclear bodies in HeLa sublines is linked to genomic rearrangements affecting chromosome 11.Chromosoma · 2016Article
- Evolution of a transcriptional regulator from a transmembrane nucleoporin.Genes & development · 2016Article
- Chromatin-prebound Crm1 recruits Nup98-HoxA9 fusion to induce aberrant expression of Hox cluster genes.eLife · 2016Article
- Expression of Leukemia-Associated Nup98 Fusion Proteins Generates an Aberrant Nuclear Envelope Phenotype.PloS one · 2016Article
- The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation.Molecular biology of the cell · 2015Article
- Intranuclear dynamics of the Nup107-160 complex.Molecular biology of the cell · 2015Article
- Nup2 requires a highly divergent partner, NupA, to fulfill functions at nuclear pore complexes and the mitotic chromatin region.Molecular biology of the cell · 2015Article
- Comparative ultrastructure of CRM1-Nucleolar bodies (CNoBs), Intranucleolar bodies (INBs) and hybrid PML/p62 bodies uncovers new facets of nuclear body dynamic and diversity.Nucleus (Austin, Tex.) · 2015Article
- New mitotic regulators released from chromatin.Frontiers in oncology · 2013Review
- In vivo analysis of human nucleoporin repeat domain interactions.Molecular biology of the cell · 2013Article
- The role of Nup98 in transcription regulation in healthy and diseased cells.Trends in cell biology · 2013Article
- POU1F1 is a novel fusion partner of NUP98 in acute myeloid leukemia with t(3;11)(p11;p15).Molecular cancer · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chromosomal translocations involving the Nup98 gene are implicated in leukemias, especially acute myelogenous leukemia. These translocations generate chimeric fusion proteins, all of which have in common the N-terminal half of Nup98, which contains the nucleoporin FG/GLFG repeat motifs. The homeodomain group of Nup98 fusion proteins retain the C-terminus of a homeodomain transcription factor, including the homeobox responsible for DNA binding. Current models for Nup98 leukemogenesis invoke aberrant transcription resulting from recruitment of coregulators by the Nup98 repeat domain. Here we have investigated the behavior of Nup98-homeodomain fusion proteins throughout the cell cycle. At all stages, the fusion proteins exhibit a novel localization distinct from the component proteins or fragments. During interphase, there are dynamic interactions between the Nup98 fusions and endogenous Nup98 that lead to mislocalization of the intranuclear fraction of Nup98, but do not alter the level of Nup98 at the nuclear pore complex. During mitosis, no interaction between the fusion proteins and endogenous Nup98 is observed. However, the fusions are entirely concentrated at kinetochores and on chromosome arms, sites where the APC/C, a target of Nup98 regulation, is also found. Our observations suggest new possibilities for misregulation by which Nup98 translocations may contribute to cellular transformation and leukemogenesis.
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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.