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Special Issue "Sphingolipids: Signals and Disease 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 30 June 2021.

Special Issue Editor

Prof. Dr. Burkhard Kleuser
E-Mail Website
Guest Editor
Department of Nutritional Toxicology, Institute of Nutritional Science, University of Potsdam, Nuthetal, Germany
Interests: sphingolipidomics; sphingosine 1-phosphate; S1P-receptors; insulin resistance; dendritic cells; epigenetics; nanotoxicology
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Special Issue Information

Dear Colleagues,

It is now well appreciated that sphingolipids are not only ubiquitous membrane lipids in eukaryotes but that they also modulate a myriad of physiological and pathophysiological processes. Sphingolipid research has grown exponentially since bioactive sphingolipid derivatives were first described just over two decades ago. Indeed, in 2010, the first sphingolipid receptor modulator, fingolimod, was employed as a human therapeutic for the treatment of multiple sclerosis. Today, it is well established that sphingolipid derivatives are critical players in immunology, inflammation, and cancer, as well as in cardiovascular and metabolic disorders. Sphingolipid research is of great complexity due to the diversity of distinct sphingolipid molecules and the interconnected metabolic pathways. The levels of sphingolipids are tightly regulated by a multitude of enzymes which are involved in the biosynthesis and degradation of sphingolipids. New knowledge on the biology and metabolism of sphingolipids is anticipated to further understand the role of this lipid class in a variety of pathophysiological conditions.

In this Special Issue, we welcome your contributions in the form of original research and review articles in all aspects of sphingolipids.

Prof. Dr. Burkhard Kleuser
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.


  • Bioactive sphingolipids
  • Ceramides
  • Sphingosine 1-phosphate
  • S1P receptors
  • Sphingolipid Metabolism
  • Sphingolipids and metabolic disorders
  • Sphingolipids and inflammation
  • Sphingolipids and infections
  • Sphingolipids and cancer

Published Papers (1 paper)

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Open AccessArticle
Identification of SYS1 as a Host Factor Required for Shiga Toxin-Mediated Cytotoxicity in Vero Cells
Int. J. Mol. Sci. 2021, 22(9), 4936; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094936 - 06 May 2021
Viewed by 193
Shiga toxin (STx) or Vero toxin is a virulence factor produced by enterohemorrhagic Escherichia coli. The toxin binds to the glycosphingolipid globotriaosylceramide (Gb3) for its entry, and causes cell death by inhibiting ribosome function. Previously, we performed a loss-of-function screen in HeLa [...] Read more.
Shiga toxin (STx) or Vero toxin is a virulence factor produced by enterohemorrhagic Escherichia coli. The toxin binds to the glycosphingolipid globotriaosylceramide (Gb3) for its entry, and causes cell death by inhibiting ribosome function. Previously, we performed a loss-of-function screen in HeLa cells using a human CRISPR knockout (KO) library and identified various host genes required for STx-induced cell death. To determine whether this library targeted to the human genome is applicable to non-human primate cells and to identify previously unrecognized factors crucial for STx-induced cell death, we herein performed a similar screen in the African green monkey kidney-derived Vero C1008 subline. Many genes relevant to metabolic enzymes and membrane trafficking were enriched, although the number of enriched genes was less than that obtained in the screening for HeLa cells. Of note, several genes that had not been enriched in the previous screening were enriched: one of these genes was SYS1, which encodes a multi-spanning membrane protein in the Golgi apparatus. In SYS1 KO Vero cells, expression of Gb3 and sphingomyelin was decreased, while that of glucosylceramide and lactosylceramide was increased. In addition, loss of SYS1 inhibited the biosynthesis of protein glycans, deformed the Golgi apparatus, and perturbed the localization of trans-Golgi network protein (TGN) 46. These results indicate that the human CRISPR KO library is applicable to Vero cell lines, and SYS1 has a widespread effect on glycan biosynthesis via regulation of intra-Golgi and endosome–TGN retrograde transports. Full article
(This article belongs to the Special Issue Sphingolipids: Signals and Disease 2.0)
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