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Protein Kinases in Cardiovascular Pathophysiology
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Protein Kinases in Cardiovascular Pathophysiology

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiology".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 3615

Special Issue Editor

Dr. Julius Bogomolovas

E-Mail Website
Guest Editor
UCSD School of Medicine, La Jolla, CA, USA
Interests: protein kinases; pseudokinases; animal models in cardiovascular research; structural biology

Special Issue Information

Dear Colleagues,

We want to draw your attention to a Special Issue focused on Kinases in Cardiovascular Pathophysiology. Kinases and pseudokinases organize a wide range of cellular processes and play integral roles in cardiovascular development, function, and disease, making them attractive therapeutic targets. Dysregulation of kinase signaling has been reported in virtually every cardiovascular pathology, ranging from heart failure with reduced ejection fraction, heart failure with preserved ejection, congenital heart defects, myocardial infarction, and inherited cardiomyopathies to atherosclerosis, hypertension, stroke, and drug cardiotoxicity.

Kinase activity in cardiomyocytes, but also in endothelial cells, fibroblasts, and immune cells, has been shown to play an active role in cardiovascular pathophysiology. A comprehensive understanding of kinases in cardiovascular health and disease requires studies on molecular, cellular, organismal, and populational levels, utilizing experimental models and clinical data.

Therefore, all the research and advances on kinases and pseudokinases in cardiac (patho)physiology are welcome in this Special Issue. Original articles, comprehensive and critical reviews, and even letters are of utmost interest, given the broad interest in this area.

Dr. Julius Bogomolovas
Guest Editor

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. Journal of Clinical Medicine 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 2600 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

  • Protein kinase C superfamily
  • Mechanosensing kinases
  • Small GTPase activated kinases
  • Cardiovascular inflammation and remodeling
  • Cardiotoxicity of kinase inhibitors
  • Pseudokinases
  • Lipid kinases
  • Kinases in heart development
  • Kinase inhibitors as therapeutic agents

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Published Papers (1 paper)

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Research

16 pages, 3374 KiB  
Article
Exploring Obscurin and SPEG Kinase Biology
by Jennifer R. Fleming, Alankrita Rani, Jamie Kraft, Sanja Zenker, Emma Börgeson and Stephan Lange
J. Clin. Med. 2021, 10(5), 984; https://doi.org/10.3390/jcm10050984 - 2 Mar 2021
Cited by 9 | Viewed by 3132
Abstract
Three members of the obscurin protein family that contain tandem kinase domains with important signaling functions for cardiac and striated muscles are the giant protein obscurin, its obscurin-associated kinase splice isoform, and the striated muscle enriched protein kinase (SPEG). While there is increasing [...] Read more.
Three members of the obscurin protein family that contain tandem kinase domains with important signaling functions for cardiac and striated muscles are the giant protein obscurin, its obscurin-associated kinase splice isoform, and the striated muscle enriched protein kinase (SPEG). While there is increasing evidence for the specific roles that each individual kinase domain plays in cross-striated muscles, their biology and regulation remains enigmatic. Our present study focuses on kinase domain 1 and the adjacent low sequence complexity inter-kinase domain linker in obscurin and SPEG. Using Phos-tag gels, we show that the linker in obscurin contains several phosphorylation sites, while the same region in SPEG remained unphosphorylated. Our homology modeling, mutational analysis and molecular docking demonstrate that kinase 1 in obscurin harbors all key amino acids important for its catalytic function and that actions of this domain result in autophosphorylation of the protein. Our bioinformatics analyses also assign a list of putative substrates for kinase domain 1 in obscurin and SPEG, based on the known and our newly proposed phosphorylation sites in muscle proteins, including obscurin itself. Full article
(This article belongs to the Special Issue Protein Kinases in Cardiovascular Pathophysiology)
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