Next Issue
Previous Issue

Table of Contents

Cells, Volume 3, Issue 1 (March 2014), Pages 1-179

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Readerexternal link to open them.
View options order results:
result details:
Displaying articles 1-9
Export citation of selected articles as:

Editorial

Jump to: Research, Review

Open AccessEditorial Acknowledgement to Reviewers of Cells in 2013
Cells 2014, 3(1), 150-151; doi:10.3390/cells3010150
Received: 25 February 2014 / Accepted: 25 February 2014 / Published: 25 February 2014
PDF Full-text (108 KB) | HTML Full-text | XML Full-text
Abstract The editors of Cells would like to express their sincere gratitude to the following reviewers for assessing manuscripts in 2013. [...] Full article

Research

Jump to: Editorial, Review

Open AccessArticle Macroscopic Quantum-Type Potentials in Theoretical Systems Biology
Cells 2014, 3(1), 1-35; doi:10.3390/cells3010001
Received: 27 July 2013 / Revised: 18 November 2013 / Accepted: 28 November 2013 / Published: 30 December 2013
Cited by 1 | PDF Full-text (1340 KB) | HTML Full-text | XML Full-text
Abstract
We review in this paper the use of the theory of scale relativity and fractal space-time as a tool particularly well adapted to the possible development of a future genuine systems theoretical biology. We emphasize in particular the concept of quantum-type potentials, [...] Read more.
We review in this paper the use of the theory of scale relativity and fractal space-time as a tool particularly well adapted to the possible development of a future genuine systems theoretical biology. We emphasize in particular the concept of quantum-type potentials, since, in many situations, the effect of the fractality of space—or of the underlying medium—can be reduced to the addition of such a potential energy to the classical equations of motion. Various equivalent representations—geodesic, quantum-like, fluid mechanical, stochastic—of these equations are given, as well as several forms of generalized quantum potentials. Examples of their possible intervention in high critical temperature superconductivity and in turbulence are also described, since some biological processes may be similar in some aspects to these physical phenomena. These potential extra energy contributions could have emerged in biology from the very fractal nature of the medium, or from an evolutive advantage, since they involve spontaneous properties of self-organization, morphogenesis, structuration and multi-scale integration. Finally, some examples of applications of the theory to actual biological-like processes and functions are also provided. Full article
(This article belongs to the Special Issue Feature Papers 2013)
Figures

Open AccessArticle Development of a Novel BAFF Responsive Cell Line Suitable for Detecting Bioactive BAFF and Neutralizing Antibodies against BAFF-Pathway Inhibiting Therapeutics
Cells 2014, 3(1), 79-91; doi:10.3390/cells3010079
Received: 12 December 2013 / Revised: 5 January 2014 / Accepted: 28 January 2014 / Published: 10 February 2014
Cited by 3 | PDF Full-text (643 KB) | HTML Full-text | XML Full-text
Abstract
BAFF has a critical role in B-cell survival, maturation and function, which makes its pathway a prime therapeutic target for various autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis and Sjögren’s syndrome. A cell-based assay that measures the functional activity [...] Read more.
BAFF has a critical role in B-cell survival, maturation and function, which makes its pathway a prime therapeutic target for various autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis and Sjögren’s syndrome. A cell-based assay that measures the functional activity of BAFF is required for many high throughput purposes, such as lead target screening and BAFF quantification. We report here the development of a sensitive BAFF responsive cell line via stable transfection of the BAFFR-TNFR1 hybrid receptor into monkey kidney epithelial COS-1 cells. The cellular response to BAFF can be detected by measuring the secretion of IL-8. This BAFF bioassay is not only reproducible and sensitive, but also responsive to a wide concentration range of BAFF stimulation in sera from various species. This cell line is useful in the development of sensitive bioassays to measure the levels of bioactive BAFF, inhibition of BAFF and neutralizing antibodies against any BAFF pathway-mediated therapeutic proteins. Full article

Review

Jump to: Editorial, Research

Open AccessReview Glucocorticoid Induced Cerebellar Toxicity in the Developing Neonate: Implications for Glucocorticoid Therapy during Bronchopulmonary Dysplasia
Cells 2014, 3(1), 36-52; doi:10.3390/cells3010036
Received: 5 December 2013 / Revised: 25 December 2013 / Accepted: 25 December 2013 / Published: 8 January 2014
Cited by 4 | PDF Full-text (3826 KB) | HTML Full-text | XML Full-text
Abstract
Prematurely born infants commonly suffer respiratory dysfunction due to the immature state of their lungs. As a result, clinicians often administer glucocorticoid (GC) therapy to accelerate lung maturation and reduce inflammation. Unfortunately, several studies have found GC therapy can also produce neuromotor/cognitive [...] Read more.
Prematurely born infants commonly suffer respiratory dysfunction due to the immature state of their lungs. As a result, clinicians often administer glucocorticoid (GC) therapy to accelerate lung maturation and reduce inflammation. Unfortunately, several studies have found GC therapy can also produce neuromotor/cognitive deficits and selectively stunt the cerebellum. However, despite its continued use, relatively little is known about how exposure to this hormone might produce neurodevelopmental deficits. In this review, we use rodent and human research to provide evidence that GC therapy may disrupt cerebellar development through the rapid induction of apoptosis in the cerebellar external granule layer (EGL). The EGL is a transient proliferative region responsible for the production of over 90% of the neurons in the cerebellum. During normal development, endogenous GC stimulation is thought to selectively signal the elimination of the EGL once production of new neurons is complete. As a result, GC therapy may precociously eliminate the EGL before it can produce enough neurons for normal cerebellar function. It is hoped that this review may provide information for future clinical research in addition to translational guidance for the safer use of GC therapy. Full article
(This article belongs to the Special Issue Apoptosis)
Open AccessReview When Good Turns Bad: Regulation of Invasion and Metastasis by ErbB2 Receptor Tyrosine Kinase
Cells 2014, 3(1), 53-78; doi:10.3390/cells3010053
Received: 25 November 2013 / Revised: 14 January 2014 / Accepted: 20 January 2014 / Published: 27 January 2014
Cited by 4 | PDF Full-text (529 KB) | HTML Full-text | XML Full-text
Abstract
Overexpression and activation of ErbB2 receptor tyrosine kinase in breast cancer is strongly linked to an aggressive disease with high potential for invasion and metastasis. In addition to inducing very aggressive, metastatic cancer, ErbB2 activation mediates processes such as increased cancer cell [...] Read more.
Overexpression and activation of ErbB2 receptor tyrosine kinase in breast cancer is strongly linked to an aggressive disease with high potential for invasion and metastasis. In addition to inducing very aggressive, metastatic cancer, ErbB2 activation mediates processes such as increased cancer cell proliferation and survival and is needed for normal physiological activities, such as heart function and development of the nervous system. How does ErbB2 activation make cancer cells invasive and when? Comprehensive understanding of the cellular mechanisms leading to ErbB2-induced malignant processes is necessary for answering these questions. Here we present current knowledge about the invasion-promoting function of ErbB2 and the mechanisms involved in it. Obtaining detailed information about the “bad” behavior of ErbB2 can facilitate development of novel treatments against ErbB2-positive cancers. Full article
(This article belongs to the Special Issue Receptor Tyrosine Kinases)
Figures

Open AccessReview Unlocking Doors without Keys: Activation of Src by Truncated C-terminal Intracellular Receptor Tyrosine Kinases Lacking Tyrosine Kinase Activity
Cells 2014, 3(1), 92-111; doi:10.3390/cells3010092
Received: 22 November 2013 / Revised: 7 February 2014 / Accepted: 7 February 2014 / Published: 14 February 2014
Cited by 6 | PDF Full-text (793 KB) | HTML Full-text | XML Full-text
Abstract
One of the best examples of the renaissance of Src as an open door to cancer has been the demonstration that just five min of Src activation is sufficient for transformation and also for induction and maintenance of cancer stem cells [1]. [...] Read more.
One of the best examples of the renaissance of Src as an open door to cancer has been the demonstration that just five min of Src activation is sufficient for transformation and also for induction and maintenance of cancer stem cells [1]. Many tyrosine kinase receptors, through the binding of their ligands, become the keys that unlock the structure of Src and activate its oncogenic transduction pathways. Furthermore, intracellular isoforms of these receptors, devoid of any tyrosine kinase activity, still retain the ability to unlock Src. This has been shown with a truncated isoform of KIT (tr-KIT) and a truncated isoform of VEGFR-1 (i21-VEGFR-1), which are intracellular and require no ligand binding, but are nonetheless able to activate Src and induce cell migration and invasion of cancer cells. Expression of the i21-VEGFR-1 is upregulated by the Notch signaling pathway and repressed by miR-200c and retinoic acid in breast cancer cells. Both Notch inhibitors and retinoic acid have been proposed as potential therapies for invasive breast cancer. Full article
(This article belongs to the Special Issue Receptor Tyrosine Kinases)
Figures

Open AccessReview Loss of TRPV2 Homeostatic Control of Cell Proliferation Drives Tumor Progression
Cells 2014, 3(1), 112-128; doi:10.3390/cells3010112
Received: 19 December 2013 / Revised: 22 January 2014 / Accepted: 8 February 2014 / Published: 19 February 2014
Cited by 3 | PDF Full-text (297 KB) | HTML Full-text | XML Full-text | Correction
Abstract
Herein we evaluate the involvement of the TRPV2 channel, belonging to the Transient Receptor Potential Vanilloid channel family (TRPVs), in development and progression of different tumor types. In normal cells, the activation of TRPV2 channels by growth factors, hormones, and endocannabinoids induces [...] Read more.
Herein we evaluate the involvement of the TRPV2 channel, belonging to the Transient Receptor Potential Vanilloid channel family (TRPVs), in development and progression of different tumor types. In normal cells, the activation of TRPV2 channels by growth factors, hormones, and endocannabinoids induces a translocation of the receptor from the endosomal compartment to the plasma membrane, which results in abrogation of cell proliferation and induction of cell death. Consequently, loss or inactivation of TRPV2 signaling (e.g., glioblastomas), induces unchecked proliferation, resistance to apoptotic signals and increased resistance to CD95-induced apoptotic cell death. On the other hand, in prostate cancer cells, Ca2+-dependent activation of TRPV2 induced by lysophospholipids increases the invasion of tumor cells. In addition, the progression of prostate cancer to the castration-resistant phenotype is characterized by de novo TRPV2 expression, with higher TRPV2 transcript levels in patients with metastatic cancer. Finally, TRPV2 functional expression in tumor cells can also depend on the presence of alternative splice variants of TRPV2 mRNA that act as dominant-negative mutant of wild-type TRPV2 channels, by inhibiting its trafficking and translocation to the plasma membrane. In conclusion, as TRP channels are altered in human cancers, and their blockage impair tumor progression, they appear to be a very promising targets for early diagnosis and chemotherapy. Full article
(This article belongs to the Special Issue Transient Receptor Potential (TRP) Channels)
Open AccessReview Flotillins in Receptor Tyrosine Kinase Signaling and Cancer
Cells 2014, 3(1), 129-149; doi:10.3390/cells3010129
Received: 11 December 2013 / Revised: 11 February 2014 / Accepted: 12 February 2014 / Published: 19 February 2014
Cited by 11 | PDF Full-text (502 KB) | HTML Full-text | XML Full-text
Abstract
Flotillins are highly conserved proteins that localize into specific cholesterol rich microdomains in cellular membranes. They have been shown to be associated with, for example, various signaling pathways, cell adhesion, membrane trafficking and axonal growth. Recent findings have revealed that flotillins are [...] Read more.
Flotillins are highly conserved proteins that localize into specific cholesterol rich microdomains in cellular membranes. They have been shown to be associated with, for example, various signaling pathways, cell adhesion, membrane trafficking and axonal growth. Recent findings have revealed that flotillins are frequently overexpressed in various types of human cancers. We here review the suggested functions of flotillins during receptor tyrosine kinase signaling and in cancer. Although flotillins have been implicated as putative cancer therapy targets, we here show that great caution is required since flotillin ablation may result in effects that increase instead of decrease the activity of specific signaling pathways. On the other hand, as flotillin overexpression appears to be related with metastasis formation in certain cancers, we also discuss the implications of these findings for future therapy aspects. Full article
(This article belongs to the Special Issue Receptor Tyrosine Kinases)
Figures

Open AccessReview Molecular Perspectives for mu/delta Opioid Receptor Heteromers as Distinct, Functional Receptors
Cells 2014, 3(1), 152-179; doi:10.3390/cells3010152
Received: 20 December 2013 / Revised: 14 February 2014 / Accepted: 21 February 2014 / Published: 5 March 2014
Cited by 9 | PDF Full-text (479 KB) | HTML Full-text | XML Full-text
Abstract
Opioid receptors are the sites of action for morphine and the other opioid drugs. Abundant evidence now demonstrates that different opioid receptor types can physically associate to form heteromers. Understandings of the nature, behavior, and role of these opioid receptor heteromers are [...] Read more.
Opioid receptors are the sites of action for morphine and the other opioid drugs. Abundant evidence now demonstrates that different opioid receptor types can physically associate to form heteromers. Understandings of the nature, behavior, and role of these opioid receptor heteromers are developing. Owing to their constituent monomers’ involvement in analgesia, mu/delta opioid receptor (M/DOR) heteromers have been a particular focus of attention. There is now considerable evidence demonstrating M/DOR to be an extant and physiologically relevant receptor species. Participating in the cellular environment as a distinct receptor type, M/DOR availability is complexly regulated and M/DOR exhibits unique pharmacology from that of other opioid receptors (ORs), including its constituents. M/DOR appears to have a range of actions that vary in a ligand- (or ligands-) dependent manner. These actions can meaningfully affect the clinical effects of opioid drugs: strategies targeting M/DOR may be therapeutically useful. This review presents and discusses developments in these understandings with a focus on the molecular nature and activity of M/DOR in the context of therapeutic potentials. Full article
(This article belongs to the Special Issue Oligomerization & Trafficking of Opioid Receptors)

Journal Contact

MDPI AG
Cells Editorial Office
St. Alban-Anlage 66, 4052 Basel, Switzerland
cells@mdpi.com
Tel. +41 61 683 77 34
Fax: +41 61 302 89 18
Editorial Board
Contact Details Submit to Cells
Back to Top