Evidence map›Paper›PMID 23730213›Full record

Observational studyNeoplasia (New York, N.Y.)2013

ERK5/BMK1 is a novel target of the tumor suppressor VHL: implication in clear cell renal carcinoma.

Laura Arias-González, Inmaculada Moreno-Gimeno, Antonio Rubio del Campo, Leticia Serrano-Oviedo, María Llanos Valero, Azucena Esparís-Ogando, Miguel Ángel de la Cruz-Morcillo, Pedro Melgar-Rojas, Jesús García-Cano, Francisco José Cimas and 9 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Oncogenic signaling of MEK5-ERK5.Cancer letters · 2017
    Review
  19. ERK5 and Cell Proliferation: Nuclear Localization Is What Matters.Frontiers in cell and developmental biology · 2016
    Review
  20. Article
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

19 authors at 6 institutions in 1 country.

Laura Arias-GonzálezLaboratorio de Oncología Molecular, Centro Regional de Investigaciones Biomédicas/University of Castilla la Mancha CRIB/UCLM, Albacete, Spain.
Inmaculada Moreno-Gimeno
Antonio Rubio del Campo
Leticia Serrano-Oviedo
María Llanos Valero
Azucena Esparís-Ogando
Miguel Ángel de la Cruz-Morcillo
Pedro Melgar-Rojas
Jesús García-Cano
Francisco José Cimas
María José Ruiz Hidalgo
Alfonso Prado
Juan Luis Callejas-Valera
Syong Hyun Nam-Cha
José Miguel Giménez-Bachs
Antonio S Salinas-Sánchez
Atanasio Pandiella
Luis del Peso
Ricardo Sánchez-Prieto
University of Castilla-La Mancha · ESHospital General Universitario de Albacete · ESComplejo Hospitalario Universitario de Albacete · ESConsejo Superior de Investigaciones Científicas · ESInstituto de Investigaciones Biomédicas Sols-Morreale · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular signal-regulated kinase 5 (ERK5), also known as big mitogen-activated protein kinase (MAPK) 1, is implicated in a wide range of biologic processes, which include proliferation or vascularization. Here, we show that ERK5 is degraded through the ubiquitin-proteasome system, in a process mediated by the tumor suppressor von Hippel-Lindau (VHL) gene, through a prolyl hydroxylation-dependent mechanism. Our conclusions derive from transient transfection assays in Cos7 cells, as well as the study of endogenous ERK5 in different experimental systems such as MCF7, HMEC, or Caki-2 cell lines. In fact, the specific knockdown of ERK5 in pVHL-negative cell lines promotes a decrease in proliferation and migration, supporting the role of this MAPK in cellular transformation. Furthermore, in a short series of fresh samples from human clear cell renal cell carcinoma, high levels of ERK5 correlate with more aggressive and metastatic stages of the disease. Therefore, our results provide new biochemical data suggesting that ERK5 is a novel target of the tumor suppressor VHL, opening a new field of research on the role of ERK5 in renal carcinomas.

Indexed as

AdultAgedAnimalsBase SequenceCarcinoma, Renal CellCell LineCell MovementChlorocebus aethiopsCOS CellsFemaleGene Knockdown TechniquesHumansHydroxylationKidney NeoplasmsMaleMiddle AgedMitogen-Activated Protein Kinase 7Proteasome Endopeptidase ComplexUbiquitinVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID23730213
PMCPMC3664997
OpenAlexW1880561744

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.