Protein Kinase C Signalling in Health and Disease: A Commemorative Issue in Honor of Prof. Yasutomi Nishizuka

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 1465

Special Issue Editors


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Department of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, Collegium Pharmaceuticum, 3 Rokietnicka Str., 60-806 Poznan, Poland
Interests: combination chemotherapy; drug delivery; targeted therapy; cancer biology
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Department of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, Collegium Pharmaceuticum, 3 Rokietnicka Str., 60-806 Poznan, Poland
Interests: PKC epsilon; cell adhesion and migration; glioblastoma; novel anticancer compounds

Special Issue Information

Dear Colleagues,

Dr. Yasutomi Nishizuka was President and Professor Emeritus of Kobe University, Kobe, Japan. He became famous by discovering a novel protein kinase that requires membrane phospholipids and Ca+2 ions. He named it protein kinase C (PKC). Dr. Nishizuka’s study focused on various research areas, including protein synthesis and phosphorylation, tryptophan metabolism, and ADP-ribosylation. Nishizuka’s research group found that diacylglycerol, a novel second messenger generated by receptor-stimulated phosphatidylinositol hydrolysis, effectively activates PKC. This sustained activation involves long-term physiological responses such as cell proliferation and differentiation. It was also discovered that PKC is the target of phorbol ester. It has soon become clear that upon receptor stimulation, various lipids in the membranes are metabolized to generate various lipid mediators, which may participate in the activation and translocation of specific PKC subtypes.

This research laid the foundation for an enormous number of studies on the complex PKC family, many of them orginating from Nishizuka's group. The discovery of PKC contributed significantly to understanding PKC-mediated signaling, as mentioned above, and establishing the importance of lipids in signal transduction. The activity of PKC family members is precisely controlled, and they finely balance cell survival with cell death pathways. Thus, their deregulation is associated with various diseases, including metabolic disorders, cancer, and neurodegeneration.

This Commemorative Special Issue seeks to honor the great researcher Dr. Yasutomi Nishizuka and his contribution to understanding the dynamic aspects of normal and pathological cell control. We solicit contributions in the form of original research articles and reviews describing the role of protein kinase C (PKC) isozymes in cellular processes such as apoptosis, autophagy, migration, and proliferation, as well as their involvement in various diseases, including metabolic disorders, cancer, and neurodegeneration.

Dr. Aleksandra Romaniuk-Drapała
Dr. Ewa Totoń
Guest Editors

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Keywords

  • novel signaling mechanisms
  • cell metabolism
  • omnics/signaling
  • immunity
  • cancer
  • neurobiology

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Published Papers (1 paper)

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Review

11 pages, 851 KiB  
Review
PKCδ Protects against Lupus Autoimmunity
by Sailee Vijay Chavan, Shreya Desikan, Christopher A J Roman and Chongmin Huan
Biomedicines 2024, 12(6), 1364; https://doi.org/10.3390/biomedicines12061364 - 19 Jun 2024
Viewed by 930
Abstract
Protein kinase C delta (PKCδ) has emerged as a key protective molecule against systemic lupus erythematosus (SLE or lupus), an autoimmune disease characterized by anti-double stranded (ds) DNA IgGs. Although PKCδ-deficient mice and lupus patients with mutated PRKCD genes clearly demonstrate the requirement [...] Read more.
Protein kinase C delta (PKCδ) has emerged as a key protective molecule against systemic lupus erythematosus (SLE or lupus), an autoimmune disease characterized by anti-double stranded (ds) DNA IgGs. Although PKCδ-deficient mice and lupus patients with mutated PRKCD genes clearly demonstrate the requirement for PKCδ in preventing lupus autoimmunity, this critical tolerance mechanism remains poorly understood. We recently reported that PKCδ acts as a key regulator of B cell tolerance by selectively deleting anti-dsDNA B cells in the germinal center (GC). PKCδ’s tolerance function is activated by sphingomyelin synthase 2 (SMS2), a lipid enzyme whose expression is generally reduced in B cells from lupus patients. Moreover, pharmacologic strengthening of the SMS2/PKCδ tolerance pathway alleviated lupus pathogenesis in mice. Here, we review relevant publications in order to provide mechanistic insights into PKCδ’s tolerance activity and discuss the potential significance of therapeutically targeting PKCδ’s tolerance activity in the GC for selectively inhibiting lupus autoimmunity. Full article
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