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Cells
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The ERK5 Signaling Pathway in Health and Disease
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The ERK5 Signaling Pathway in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (10 October 2023) | Viewed by 4823

Special Issue Editors

Dr. Michael Cross

E-Mail Website
Guest Editor
Department of Molecular and Clinical Pharmacology, MRC Centre for Drug Safety Science, Institute of Translational Medicine, University of Liverpool, Sherrington Building, Liverpool L69 3GE, UK
Interests: ERK5 signaling; endothelial cells; cardioprotection
Special Issues, Collections and Topics in MDPI journals
Dr. Elisabetta Rovida

E-Mail Website
Guest Editor
Dipartimento di Scienze Biomediche, Sperimentali e Cliniche, University of Florence, Florence, Italy
Interests: MAPK; targeted therapy; cancer; ERK5; cell signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Jose M. Lizcano

E-Mail Website
Guest Editor
1. Department of Biochemistry, Institute of Neurosciences, Faculty of Medicine, University Autonoma de Barcelona, Bellaterra, 08193 Barcelona, Spain
2. Vall d'Hebron Research Institute (VHIR), 08035 Barcelona, Spain
Interests: protein kinases; cell signaling; cancer; anticancer drugs

Special Issue Information

Dear Colleagues,

ERK5, the last MAP kinase family member to be discovered, is activated by the upstream kinase MEK5 in response to a range of growth factors and stress stimulation. The ERK5 signaling axis has been shown to regulate a number of different cellular processes in cells, ranging from endothelial cells lining blood vessels to neuronal cells in the central nervous system and embryonic stem cells as well as a multitude of different cancer cells.  

Following on from the first international conference on ERK5 signaling in July 2022 in Barcelona, we want to focus this Special Issue on the role and regulation of this enigmatic kinase in a range of different cells. We aim to capture the scope of ongoing research to elucidate the role of ERK5 in human physiology and pathophysiology and the potential therapeutic opportunities presented by modulating the activation of this kinase.

Dr. Michael Cross
Dr. Elisabetta Rovida
Dr. Jose M. Lizcano
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Extracellular-Regulated Kinase 5 (ERK5)
  • Mitogen-Activated Protein Kinase (MAPK)
  • cancer
  • kinase inhibitors
  • endothelial cells
  • stem cells

Published Papers (2 papers)

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Research

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18 pages, 4693 KiB  
Article
VEGF Stimulates Activation of ERK5 in the Absence of C-Terminal Phosphorylation Preventing Nuclear Localization and Facilitating AKT Activation in Endothelial Cells
by Anil Kumar Mondru, Mohammad A. Aljasir, Ahmed Alrumayh, Gopika N. Nithianandarajah, Katie Ahmed, Jurgen Muller, Christopher E. P. Goldring, Bettina Wilm and Michael J. Cross
Cells 2023, 12(6), 967; https://doi.org/10.3390/cells12060967 - 22 Mar 2023
Viewed by 2029
Abstract
Extracellular-signal-regulated kinase 5 (ERK5) is critical for normal cardiovascular development. Previous studies have defined a canonical pathway for ERK5 activation, showing that ligand stimulation leads to MEK5 activation resulting in dual phosphorylation of ERK5 on Thr218/Tyr220 residues within the activation loop. ERK5 then [...] Read more.
Extracellular-signal-regulated kinase 5 (ERK5) is critical for normal cardiovascular development. Previous studies have defined a canonical pathway for ERK5 activation, showing that ligand stimulation leads to MEK5 activation resulting in dual phosphorylation of ERK5 on Thr218/Tyr220 residues within the activation loop. ERK5 then undergoes a conformational change, facilitating phosphorylation on residues in the C-terminal domain and translocation to the nucleus where it regulates MEF2 transcriptional activity. Our previous research into the importance of ERK5 in endothelial cells highlighted its role in VEGF-mediated tubular morphogenesis and cell survival, suggesting that ERK5 played a unique role in endothelial cells. Our current data show that in contrast to EGF-stimulated HeLa cells, VEGF-mediated ERK5 activation in human dermal microvascular endothelial cells (HDMECs) does not result in C-terminal phosphorylation of ERK5 and translocation to the nucleus, but instead to a more plasma membrane/cytoplasmic localisation. Furthermore, the use of small-molecule inhibitors to MEK5 and ERK5 shows that instead of regulating MEF2 activity, VEGF-mediated ERK5 is important for regulating AKT activity. Our data define a novel pathway for ERK5 activation in endothelial cells leading to cell survival. Full article
(This article belongs to the Special Issue The ERK5 Signaling Pathway in Health and Disease)
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Review

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23 pages, 866 KiB  
Review
Pathophysiological Impact of the MEK5/ERK5 Pathway in Oxidative Stress
by Ignazia Tusa, Alessio Menconi, Alessandro Tubita and Elisabetta Rovida
Cells 2023, 12(8), 1154; https://doi.org/10.3390/cells12081154 - 13 Apr 2023
Cited by 5 | Viewed by 2032
Abstract
Oxidative stress regulates many physiological and pathological processes. Indeed, a low increase in the basal level of reactive oxygen species (ROS) is essential for various cellular functions, including signal transduction, gene expression, cell survival or death, as well as antioxidant capacity. However, if [...] Read more.
Oxidative stress regulates many physiological and pathological processes. Indeed, a low increase in the basal level of reactive oxygen species (ROS) is essential for various cellular functions, including signal transduction, gene expression, cell survival or death, as well as antioxidant capacity. However, if the amount of generated ROS overcomes the antioxidant capacity, excessive ROS results in cellular dysfunctions as a consequence of damage to cellular components, including DNA, lipids and proteins, and may eventually lead to cell death or carcinogenesis. Both in vitro and in vivo investigations have shown that activation of the mitogen-activated protein kinase kinase 5/extracellular signal-regulated kinase 5 (MEK5/ERK5) pathway is frequently involved in oxidative stress-elicited effects. In particular, accumulating evidence identified a prominent role of this pathway in the anti-oxidative response. In this respect, activation of krüppel-like factor 2/4 and nuclear factor erythroid 2-related factor 2 emerged among the most frequent events in ERK5-mediated response to oxidative stress. This review summarizes what is known about the role of the MEK5/ERK5 pathway in the response to oxidative stress in pathophysiological contexts within the cardiovascular, respiratory, lymphohematopoietic, urinary and central nervous systems. The possible beneficial or detrimental effects exerted by the MEK5/ERK5 pathway in the above systems are also discussed. Full article
(This article belongs to the Special Issue The ERK5 Signaling Pathway in Health and Disease)
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