Evidence map›Paper›PMID 26740045›Full record

ArticleeLife2016

Chromatin-prebound Crm1 recruits Nup98-HoxA9 fusion to induce aberrant expression of Hox cluster genes.

Masahiro Oka, Sonoko Mura, Kohji Yamada, Percival Sangel, Saki Hirata, Kazumitsu Maehara, Koichi Kawakami, Taro Tachibana, Yasuyuki Ohkawa, Hiroshi Kimura and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

58 citing papers in PubMed, 79 citations in OpenAlex.

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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

11 authors at 6 institutions in 1 country.

Masahiro OkaLaboratory of Nuclear Transport Dynamics, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka, Japan.
Sonoko MuraGraduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Kohji YamadaLaboratory of Nuclear Transport Dynamics, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka, Japan.
Percival SangelLaboratory of Nuclear Transport Dynamics, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka, Japan.
Saki HirataDepartment of Advanced Medical Initiatives, Kyushu University, Fukuoka, Japan.
Kazumitsu MaeharaDepartment of Advanced Medical Initiatives, Kyushu University, Fukuoka, Japan.
Koichi KawakamiDivision of Molecular and Developmental Biology, National Institute of Genetics, Shizuoka, Japan.
Taro TachibanaDepartment of Bioengineering, Osaka City University, Graduate School of Engineering, Osaka, Japan.
Yasuyuki OhkawaDepartment of Advanced Medical Initiatives, Kyushu University, Fukuoka, Japan.
Hiroshi KimuraDepartment of Biological Sciences, Graduate School of Bioscience and Technology, Tokyo Institute of Technology, Yokohama, Japan.ORCID http://orcid.org/0000-0003-0854-083X
Yoshihiro YonedaLaboratory of Biomedical Innovation, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
National Institute of Biomedical Innovation, Health and Nutrition · JPKyushu University · JPNational Institute of Genetics · JPOsaka City University · JPTokyo Institute of Technology · JPUbe Frontier University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nucleoporin Nup98 is frequently rearranged to form leukemogenic Nup98-fusion proteins with various partners. However, their function remains largely elusive. Here, we show that Nup98-HoxA9, a fusion between Nup98 and the homeobox transcription factor HoxA9, forms nuclear aggregates that frequently associate with facultative heterochromatin. We demonstrate that stable expression of Nup98-HoxA9 in mouse embryonic stem cells selectively induces the expression of Hox cluster genes. Genome-wide binding site analysis revealed that Nup98-HoxA9 is preferentially targeted and accumulated at Hox cluster regions where the export factor Crm1 is originally prebound. In addition, leptomycin B, an inhibitor of Crm1, disassembled nuclear Nup98-HoxA9 dots, resulting in the loss of chromatin binding of Nup98-HoxA9 and Nup98-HoxA9-mediated activation of Hox genes. Collectively, our results indicate that highly selective targeting of Nup98-fusion proteins to Hox cluster regions via prebound Crm1 induces the formation of higher order chromatin structures that causes aberrant Hox gene regulation.

Indexed as

Gene Expression RegulationAnimalsCell LineChromatinEmbryonic Stem CellsExportin 1 ProteinHomeodomain ProteinsHumansKaryopherinsMiceNuclear Pore Complex ProteinsProtein BindingReceptors, Cytoplasmic and NuclearChromatinExportin 1 Proteinhomeobox protein HOXA9Homeodomain ProteinsKaryopherinsNuclear Pore Complex ProteinsNup98 protein, humanReceptors, Cytoplasmic and Nuclearcell biologyChromatinchromosomesCrm1genesHoxhumanLeukemiamouseNucleoporinNup98

Identifiers

PMID26740045
PMCPMC4718815
OpenAlexW2227904090

What OpenQuestion holds

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LicenceCC BY
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.