scholarly journals The Art of Mast Cell Adhesion

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2664
Author(s):  
Joanna Pastwińska ◽  
Paulina Żelechowska ◽  
Aurelia Walczak-Drzewiecka ◽  
Ewa Brzezińska-Błaszczyk ◽  
Jarosław Dastych
Keyword(s):  
Cell Adhesion ◽  
Current Knowledge ◽  
Living Organism ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Adhesion Sites ◽  
Inflammatory Processes ◽  
Adhesive Molecules ◽  
Adhesive Proteins ◽  
Insight Into

Cell adhesion is one of the basic phenomena occurring in a living organism, affecting many other processes such as proliferation, differentiation, migration, or cell viability. Mast cells (MCs) are important elements involved in defending the host against various pathogens and regulating inflammatory processes. Due to numerous mediators, they are contributing to the modulation of many basic cellular processes in a variety of cells, including the expression and functioning of different adhesive molecules. They also express themselves many adhesive proteins, including ICAM-1, ICAM-3, VCAM-1, integrins, L-selectin, E-cadherin, and N-cadherin. These molecules enable MCs to interact with other cells and components of the extracellular matrix (ECM), creating structures such as adherens junctions and focal adhesion sites, and triggering a signaling cascade. A thorough understanding of these cellular mechanisms can create a better understanding of MC biology and reveal new goals for MC targeted therapy. This review will focus on the current knowledge of adhesion mechanisms with the involvement of MCs. It also provides insight into the influence of MCs or MC-derived mediators on the adhesion molecule expression in different cells.

Enzymes of ubiquitination and deubiquitination

2012 ◽  
Vol 52 ◽  
pp. 37-50 ◽  
Author(s):  
Melanie Neutzner ◽  
Albert Neutzner
Keyword(s):  
Protein Trafficking ◽  
Current Knowledge ◽  
Covalent Attachment ◽  
Cellular Processes ◽  
Regulatory Processes ◽  
Substrate Protein ◽  
Ubiquitin Conjugating Enzyme ◽  
The Many ◽  
Enzymatic Machinery ◽  
Insight Into

Ubiquitination, the covalent attachment of the small protein modifier ubiquitin to a substrate protein is involved in virtually all cellular processes by mediating the regulated degradation of proteins. Aside from proteasomal degradation, ubiquitination plays important roles in transcriptional regulation, protein trafficking, including endocytosis and lysosomal targeting, and activation of kinases involved in signalling processes. A three-tiered enzymatic cascade consisting of E1 or ubiquitin-activating enzyme, E2 or ubiquitin-conjugating enzyme, and E3, or ubiquitin ligases, is necessary to achieve the many forms of ubiquitination known to date. In this chapter, we summarize the current knowledge on the enzymatic machinery necessary for ubiquitin activation and ligation, as well as its removal, and provide some insight into the complexity of regulatory processes governed by ubiquitination.

Exploiting S-nitrosylation for cancer therapy: facts and perspectives

2020 ◽  
Vol 477 (19) ◽  
pp. 3649-3672
Author(s):  
Salvatore Rizza ◽  
Giuseppe Filomeni
Keyword(s):  
Nitric Oxide ◽  
Cancer Biology ◽  
Synthetic Lethality ◽  
Current Knowledge ◽  
Tissue Homeostasis ◽  
Loss Of Function ◽  
Post Translational Modification ◽  
Cellular Processes ◽  
Insight Into

S-nitrosylation, the post-translational modification of cysteines by nitric oxide, has been implicated in several cellular processes and tissue homeostasis. As a result, alterations in the mechanisms controlling the levels of S-nitrosylated proteins have been found in pathological states. In the last few years, a role in cancer has been proposed, supported by the evidence that various oncoproteins undergo gain- or loss-of-function modifications upon S-nitrosylation. Here, we aim at providing insight into the current knowledge about the role of S-nitrosylation in different aspects of cancer biology and report the main anticancer strategies based on: (i) reducing S-nitrosylation-mediated oncogenic effects, (ii) boosting S-nitrosylation to stimulate cell death, (iii) exploiting S-nitrosylation through synthetic lethality.

scholarly journals Skeletal Muscle Deconditioning in Breast Cancer Patients Undergoing Chemotherapy: Current Knowledge and Insights From Other Cancers

2021 ◽  
Vol 9 ◽  
Author(s):  
Joris Mallard ◽  
Elyse Hucteau ◽  
Thomas J. Hureau ◽  
Allan F. Pagano
Keyword(s):  
Breast Cancer ◽  
Skeletal Muscle ◽  
Cancer Patients ◽  
Current Knowledge ◽  
Tumor Development ◽  
Disease Free Survival ◽  
Breast Cancer Patients ◽  
Cellular Mechanisms ◽  
Cross Sectional ◽  
Cellular Processes

Breast cancer represents the most commonly diagnosed cancer while neoadjuvant and adjuvant chemotherapies are extensively used in order to reduce tumor development and improve disease-free survival. However, chemotherapy also leads to severe off-target side-effects resulting, together with the tumor itself, in major skeletal muscle deconditioning. This review first focuses on recent advances in both macroscopic changes and cellular mechanisms implicated in skeletal muscle deconditioning of breast cancer patients, particularly as a consequence of the chemotherapy treatment. To date, only six clinical studies used muscle biopsies in breast cancer patients and highlighted several important aspects of muscle deconditioning such as a decrease in muscle fibers cross-sectional area, a dysregulation of protein turnover balance and mitochondrial alterations. However, in comparison with the knowledge accumulated through decades of intensive research with many different animal and human models of muscle atrophy, more studies are necessary to obtain a comprehensive understanding of the cellular processes implicated in breast cancer-mediated muscle deconditioning. This understanding is indeed essential to ultimately lead to the implementation of efficient preventive strategies such as exercise, nutrition or pharmacological treatments. We therefore also discuss potential mechanisms implicated in muscle deconditioning by drawing a parallel with other cancer cachexia models of muscle wasting, both at the pre-clinical and clinical levels.

scholarly journals mRNA Post-Transcriptional Regulation by AU-Rich Element-Binding Proteins in Liver Inflammation and Cancer

2020 ◽  
Vol 21 (18) ◽  
pp. 6648
Author(s):  
Dobrochna Dolicka ◽  
Cyril Sobolewski ◽  
Marta Correia de Sousa ◽  
Monika Gjorgjieva ◽  
Michelangelo Foti
Keyword(s):  
Liver Diseases ◽  
Binding Proteins ◽  
Current Knowledge ◽  
Cellular Processes ◽  
Complex Processes ◽  
Cellular Context ◽  
Inflammatory Processes ◽  
The Stability ◽  
And Function ◽  
Post Transcriptional Regulation

AU-rich element-binding proteins (AUBPs) represent important post-transcriptional regulators of gene expression. AUBPs can bind to the AU-rich elements present in the 3’-UTR of more than 8% of all mRNAs and are thereby able to control the stability and/or translation of numerous target mRNAs. The regulation of the stability and the translation of mRNA transcripts by AUBPs are highly complex processes that occur through multiple mechanisms depending on the cell type and the cellular context. While AUBPs have been shown to be involved in inflammatory processes and the development of various cancers, their important role and function in the development of chronic metabolic and inflammatory fatty liver diseases (FLDs), as well as in the progression of these disorders toward cancers such as hepatocellular carcinoma (HCC), has recently started to emerge. Alterations of either the expression or activity of AUBPs are indeed significantly associated with FLDs and HCC, and accumulating evidence indicates that several AUBPs are deeply involved in a significant number of cellular processes governing hepatic metabolic disorders, inflammation, fibrosis, and carcinogenesis. Herein, we discuss our current knowledge of the roles and functions of AUBPs in liver diseases and cancer. The relevance of AUBPs as potential biomarkers for different stages of FLD and HCC, or as therapeutic targets for these diseases, are also highlighted.

Nucleosome dynamics

2006 ◽  
Vol 73 ◽  
pp. 109-119 ◽  
Author(s):  
Chris Stockdale ◽  
Michael Bruno ◽  
Helder Ferreira ◽  
Elisa Garcia-Wilson ◽  
Nicola Wiechens ◽  
...  
Keyword(s):  
High Resolution ◽  
Chromatin Structure ◽  
Current Knowledge ◽  
Dynamic Properties ◽  
Structure And Dynamics ◽  
Nucleosome Dynamics ◽  
Sharp Focus ◽  
Recent Advances ◽  
Insight Into ◽  
Chromatin Structure And Dynamics

In the 30 years since the discovery of the nucleosome, our picture of it has come into sharp focus. The recent high-resolution structures have provided a wealth of insight into the function of the nucleosome, but they are inherently static. Our current knowledge of how nucleosomes can be reconfigured dynamically is at a much earlier stage. Here, recent advances in the understanding of chromatin structure and dynamics are highlighted. The ways in which different modes of nucleosome reconfiguration are likely to influence each other are discussed, and some of the factors likely to regulate the dynamic properties of nucleosomes are considered.

Fabrication of Nanoscale Hydrophobic Regions on Anodic Alumina for Selective Adhesion of Biologic Molecules

2003 ◽  
Vol 773 ◽  
Author(s):  
Xiefan Lin ◽  
Anthony S. W. Ham ◽  
Natalie A. Villani ◽  
Whye-Kei Lye ◽  
Qiyu Huang ◽  
...  
Keyword(s):  
Anodic Alumina ◽  
Biological Molecules ◽  
Spatial Density ◽  
Length Scale ◽  
Adhesion Sites ◽  
A Cell ◽  
Adhesive Molecules ◽  
Receptor Clusters ◽  
Molecular Bonding ◽  
Fabrication Parameters

AbstractStudies of selective adhesion of biological molecules provide a path for understanding fundamental cellular properties. A useful technique is to use patterned substrates, where the pattern of interest has the same length scale as the molecular bonding sites of a cell, in the tens of nanometer range. We employ electrochemical methods to grow anodic alumina, which has a naturally ordered pore structure (interpore spacing of 40 to 400 nm) controlled by the anodization potential. We have also developed methods to selectively fill the alumina pores with materials with contrasting properties. Gold, for example, is electrochemically plated into the pores, and the excess material is removed by backsputter etching. The result is a patterned surface with closely separated islands of Au, surrounded by hydrophilic alumina. The pore spacing, which is determined by fabrication parameters, is hypothesized to have a direct effect on the spatial density of adhesion sites. By attaching adhesive molecules to the Au islands, we are able to observe and study cell rolling and adhesion phenomena. Through the measurements it is possible to estimate the length scale of receptor clusters on the cell surface. This information is useful in understanding mechanisms of leukocytes adhesion to endothelial cells as well as the effect of adhesion molecules adaptation on transmission of extracellular forces. The method also has applications in tissue engineering, drug and gene delivery, cell signaling and biocompatibility design.

scholarly journals Significance of Mast Cell Formed Extracellular Traps in Microbial Defense

2021 ◽  
Author(s):  
Daniel Elieh Ali Komi ◽  
Wolfgang M. Kuebler
Keyword(s):  
State Of The Art ◽  
Extracellular Dna ◽  
Cellular Mechanisms ◽  
Extracellular Traps ◽  
Synthetic Chemicals ◽  
Dna Strands ◽  
Associated Proteins ◽  
Microbial Defense ◽  
And Function ◽  
Insight Into

AbstractMast cells (MCs) are critically involved in microbial defense by releasing antimicrobial peptides (such as cathelicidin LL-37 and defensins) and phagocytosis of microbes. In past years, it has become evident that in addition MCs may eliminate invading pathogens by ejection of web-like structures of DNA strands embedded with proteins known together as extracellular traps (ETs). Upon stimulation of resting MCs with various microorganisms, their products (including superantigens and toxins), or synthetic chemicals, MCs become activated and enter into a multistage process that includes disintegration of the nuclear membrane, release of chromatin into the cytoplasm, adhesion of cytoplasmic granules on the emerging DNA web, and ejection of the complex into the extracellular space. This so-called ETosis is often associated with cell death of the producing MC, and the type of stimulus potentially determines the ratio of surviving vs. killed MCs. Comparison of different microorganisms with specific elimination characteristics such as S pyogenes (eliminated by MCs only through extracellular mechanisms), S aureus (removed by phagocytosis), fungi, and parasites has revealed important aspects of MC extracellular trap (MCET) biology. Molecular studies identified that the formation of MCET depends on NADPH oxidase-generated reactive oxygen species (ROS). In this review, we summarize the present state-of-the-art on the biological relevance of MCETosis, and its underlying molecular and cellular mechanisms. We also provide an overview over the techniques used to study the structure and function of MCETs, including electron microscopy and fluorescence microscopy using specific monoclonal antibodies (mAbs) to detect MCET-associated proteins such as tryptase and histones, and cell-impermeant DNA dyes for labeling of extracellular DNA. Comparing the type and biofunction of further MCET decorating proteins with ETs produced by other immune cells may help provide a better insight into MCET biology in the pathogenesis of autoimmune and inflammatory disorders as well as microbial defense.

scholarly journals Stick around: Cell–Cell Adhesion Molecules during Neocortical Development

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 118
Author(s):  
David de Agustín-Durán ◽  
Isabel Mateos-White ◽  
Jaime Fabra-Beser ◽  
Cristina Gil-Sanz
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Neural Cells ◽  
Surface Receptors ◽  
Cellular Processes ◽  
Neocortical Development ◽  
Classical Cadherins ◽  
Adhesive Interactions ◽  
Cell Cell

The neocortex is an exquisitely organized structure achieved through complex cellular processes from the generation of neural cells to their integration into cortical circuits after complex migration processes. During this long journey, neural cells need to establish and release adhesive interactions through cell surface receptors known as cell adhesion molecules (CAMs). Several types of CAMs have been described regulating different aspects of neurodevelopment. Whereas some of them mediate interactions with the extracellular matrix, others allow contact with additional cells. In this review, we will focus on the role of two important families of cell–cell adhesion molecules (C-CAMs), classical cadherins and nectins, as well as in their effectors, in the control of fundamental processes related with corticogenesis, with special attention in the cooperative actions among the two families of C-CAMs.

scholarly journals Regulation of Neural Cell Adhesion Molecule Polysialylation: Evidence for Nontranscriptional Control and Sensitivity to an Intracellular Pool of Calcium

1998 ◽  
Vol 140 (5) ◽  
pp. 1177-1186 ◽  
Author(s):  
Juan L. Brusés ◽  
Urs Rutishauser
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Calcium Ionophore ◽  
Cytosolic Calcium ◽  
Neural Cell ◽  
Ciliary Ganglion ◽  
Cellular Mechanisms ◽  
Neural Cell Adhesion

The up- and downregulation of polysialic acid–neural cell adhesion molecule (PSA–NCAM) expression on motorneurons during development is associated respectively with target innervation and synaptogenesis, and is regulated at the level of PSA enzymatic biosynthesis involving specific polysialyltransferase activity. The purpose of this study has been to describe the cellular mechanisms by which that regulation might occur. It has been found that developmental regulation of PSA synthesis by ciliary ganglion motorneurons is not reflected in the levels of polysialyltransferase-1 (PST) or sialyltransferase-X (STX) mRNA. On the other hand, PSA synthesis in both the ciliary ganglion and the developing tectum appears to be coupled to the concentration of calcium in intracellular compartments. This study documents a calcium dependence of polysialyltransferase activity in a cell-free assay over the range of 0.1–1 mM, and a rapid sensitivity of new PSA synthesis, as measured in a pulse–chase analysis of tissue explants, to calcium ionophore perturbation of intracellular calcium levels. Moreover, the relevant calcium pool appears to be within a specific intracellular compartment that is sensitive to thapsigargin and does not directly reflect the level of cytosolic calcium. Perturbation of other major second messenger systems, such as cAMP and protein kinase–dependent pathways, did not affect polysialylation in the pulse chase analysis. These results suggest that the shuttling of calcium to different pools within the cell can result in the rapid regulation of PSA synthesis in developing tissues.

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