Evidence map›Paper›PMID 27090638›Full record

ArticleMolecular and cellular biology2016

Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degradation of B-Myb and Hypoxia-Inducible Factor α.

Fumihiko Okumura, Keiji Uematsu, Stuart D Byrne, Mie Hirano, Akiko Joo-Okumura, Akihiko Nishikimi, Taro Shuin, Yoshinori Fukui, Kunio Nakatsukasa, Takumi Kamura

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

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  3. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
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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

10 authors at 3 institutions in 1 country.

Fumihiko OkumuraDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan okumura.fumihiko@a.mbox.nagoya-u.ac.jp z47617a@nucc.cc.nagoya-u.ac.jp.
Keiji UematsuDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan.
Stuart D ByrneDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan.
Mie HiranoDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan.
Akiko Joo-OkumuraDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan.
Akihiko NishikimiDivision of Immunogenetics, Department of Immunobiology and Neuroscience and Research Center for Advanced Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Taro ShuinDepartment of Urology, Kochi University, Kochi, Japan.
Yoshinori FukuiDivision of Immunogenetics, Department of Immunobiology and Neuroscience and Research Center for Advanced Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Kunio NakatsukasaDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan.
Takumi KamuraDivision of Biological Science, Graduate School of Science, Nagoya University, Aichi, Japan okumura.fumihiko@a.mbox.nagoya-u.ac.jp z47617a@nucc.cc.nagoya-u.ac.jp.
Nagoya University · JPKyushu University · JPUniversity of Kochi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

pVHL, the protein product of the von Hippel-Lindau (VHL) tumor suppressor gene, is a ubiquitin ligase that targets hypoxia-inducible factor α (HIF-α) for proteasomal degradation. Although HIF-α activation is necessary for VHL disease pathogenesis, constitutive activation of HIF-α alone did not induce renal clear cell carcinomas and pheochromocytomas in mice, suggesting the involvement of an HIF-α-independent pathway in VHL pathogenesis. Here, we show that the transcription factor B-Myb is a pVHL substrate that is degraded via the ubiquitin-proteasome pathway and that vascular endothelial growth factor (VEGF)- and/or platelet-derived growth factor (PDGF)-dependent tyrosine 15 phosphorylation of B-Myb prevents its degradation. Mice injected with B-Myb knockdown 786-O cells developed dramatically larger tumors than those bearing control cell tumors. Microarray screening of B-Myb-regulated genes showed that the expression of HIF-α-dependent genes was not affected by B-Myb knockdown, indicating that B-Myb prevents HIF-α-dependent tumorigenesis through an HIF-α-independent pathway. These data indicate that the regulation of B-Myb by pVHL plays a critical role in VHL disease.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsCell Line, TumorGene Expression Regulation, NeoplasticGene Knockdown TechniquesHEK293 CellsHumansMiceNeoplasm TransplantationPhosphorylationProteasome Endopeptidase ComplexProteolysisSignal TransductionTrans-ActivatorsTyrosineBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsMYBL2 protein, humanProteasome Endopeptidase ComplexTrans-ActivatorsTyrosineUbiquitinVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID27090638
PMCPMC4907096
OpenAlexW2410015936

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.