Next Article in Journal
F13A1 Gene Variant (V34L) and Residual Circulating FXIIIA Levels Predict Short- and Long-Term Mortality in Acute Myocardial Infarction after Coronary Angioplasty
Previous Article in Journal
TOP2B: The First Thirty Years
Article Menu
Issue 9 (September) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2018, 19(9), 2767; https://doi.org/10.3390/ijms19092767

Proteasome-Rich PaCS as an Oncofetal UPS Structure Handling Cytosolic Polyubiquitinated Proteins. In Vivo Occurrence, in Vitro Induction, and Biological Role

1
Department of Molecular Medicine, University of Pavia, 27100 Pavia, Italy
2
Pathologic Anatomy Unit, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
3
Centro Grandi Strumenti, University of Pavia, 27100 Pavia, Italy
*
Author to whom correspondence should be addressed.
Received: 29 August 2018 / Accepted: 11 September 2018 / Published: 14 September 2018
(This article belongs to the Special Issue Proteostasis and Proteasome Inhibitors)
Full-Text   |   PDF [3278 KB, uploaded 14 September 2018]   |  

Abstract

In this article, we outline and discuss available information on the cellular site and mechanism of proteasome interaction with cytosolic polyubiquitinated proteins and heat-shock molecules. The particulate cytoplasmic structure (PaCS) formed by barrel-like particles, closely reproducing in vivo the high-resolution structure of 26S proteasome as isolated in vitro, has been detected in a variety of fetal and neoplastic cells, from living tissue or cultured cell lines. Specific trophic factors and interleukins were found to induce PaCS during in vitro differentiation of dendritic, natural killer (NK), or megakaryoblastic cells, apparently through activation of the MAPK-ERK pathway. Direct interaction of CagA bacterial oncoprotein with proteasome was shown inside the PaCSs of a Helicobacter pylori-infected gastric epithelium, a finding suggesting a role for PaCS in CagA-mediated gastric carcinogenesis. PaCS dissolution and autophagy were seen after withdrawal of inducing factors. PaCS-filled cell blebs and ectosomes were found in some cells and may represent a potential intercellular discharge and transport system of polyubiquitinated antigenic proteins. PaCS differs substantially from the inclusion bodies, sequestosomes, and aggresomes reported in proteinopathies like Huntington or Parkinson diseases, which usually lack PaCS. The latter seems more linked to conditions of increased cell proliferation/differentiation, implying an increased functional demand to the ubiquitin–proteasome system. View Full-Text
Keywords: proteasome; polyubiquitinated proteins; heat-shock proteins; PaCS; neoplastic cells; fetal cells; microbial oncogenic proteins; trophic factors/interleukins; sequestosomes; aggresomes proteasome; polyubiquitinated proteins; heat-shock proteins; PaCS; neoplastic cells; fetal cells; microbial oncogenic proteins; trophic factors/interleukins; sequestosomes; aggresomes
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Solcia, E.; Necchi, V.; Sommi, P.; Ricci, V. Proteasome-Rich PaCS as an Oncofetal UPS Structure Handling Cytosolic Polyubiquitinated Proteins. In Vivo Occurrence, in Vitro Induction, and Biological Role. Int. J. Mol. Sci. 2018, 19, 2767.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top