Special Issue "Receptor Tyrosine Kinases"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (15 November 2013)
Dr. Sassan Hafizi
School of Pharmacy and Biomedical Sciences, Division of Pharmacology, University of Portsmouth, UK
Interests: epigenetics; focal adhesion proteins; receptor tyrosine kinases; cell signalling; vitamin K; cancer; myelin; multiple sclerosis; brain tumours; renal carcinoma; cytoskeleton; cell migration
Since the earliest discoveries of growth factors in the 1950s and of transmembrane receptors for these factors that possess protein tyrosine kinase activity in the 1970s, the body of knowledge on receptor tyrosine kinases (RTKs) has increased appreciably. The uniqueness in structure and ligand-binding specificities of the ectodomain of RTKs determines their subclassification, and today we know of the existence of around 20 different RTK classes, with a number and diversity of ligands that is ever increasing. Despite this diversity, RTKs continue to together represent a major group of molecules that play important roles in both health and disease. Normal RTK function is associated with development, cell and tissue growth and differentiation and cell-cell and cell-matrix interaction, whereas RTK overactivity and/or overexpression is a common feature in many cancers. However, novel aspects to RTK structure and function are increasingly becoming apparent as more research is being done. Amongst these include ligand-dependent and -independent mechanisms of activation, alternative and unexpected receptor clustering patterns, spatial and temporal control of RTK signalling, intracellular RTK functions, RTKs as entry gateways for pathogens, and as highly attractive candidates in target-specific cancer therapy. The aim with this Special Issue of Cells is to offer an Open Access collection of scholarly reviews on the forefront of research on RTKs that covers all of the above aspects and more. We hope to provide a stimulating resource that will inform the student and the academic on the breadth and diversity of RTK biology. This is a field that is sure to maintain a high level of interest and research activity from both academic and industrial sectors with interests in science and medicine well into the future.
Dr. Sassan Hafizi
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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. For the first couple of issues the Article Processing Charge (APC) will be waived for well-prepared manuscripts. English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- receptor tyrosine kinases
- growth factor
- signal transduction
- spatial and temporal signalling
- tyrosine kinase domain
- transmembrane domain
- RTK class
- docking protein
- monoclonal antibodies
- small molecule inhibitors
- anti-cancer drug resistance
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: When Good Gets very Bad: Regulation of Invasion and Metastasis by ErbB2 Receptor Tyrosine Kinase
Authors: Bo Rafn and Tuula Kallunki
Affiliation: Unit of Cell Death and Metabolism, Danish Cancer Society ResearchCenter, Strandboulevarden 49, DK2100 Copenhagen, Denmark; E-Mail: email@example.com
Abstract: Overexpression and activation of ErbB2 receptor tyrosine kinase in breast cancer is stronglylinked to an aggressive disease with high potential for invasion and metastasis. In addition to inducing very aggressive, metastatic cancer, ErbB2 activation also mediates processes such as increased cancer cell proliferation and survival and is needed for normal physiological activities like heart function and development of the nervous system. How does ErbB2 activation then make cancer cells metastatic and when? The proper understanding of the cellular mechanisms leading to the ErbB2-induced malignant processes is necessary for answering these questions. This can be achieved by dissecting the good and bad signals mediated by ErbB2 activation. Here we present the current knowledge about the issue and discuss the advances this can make in the development of treatments against ErbB2-positive cancers.
Type of Paper: Review
Title: Monomers, Dimers or Tetramers: Mechanisms of Activation of Receptor Tyrosine Kinases
Author: Ichiro N. Maruyama
Affiliation: Information Processing Biology Unit, Okinawa Institute of Science and Technology, Graduate University, 1919-1 Tancha, Onna-son, Kunigami, Okinawa 904-0495, Japan; E-Mail: firstname.lastname@example.org
Abstract: Receptor tyrosine kinases (RTKs) play essential roles in cellular processes including metabolism, cell-cycle control, survival, proliferation, motility and differentiation. All RTKs are single-pass transmembrane proteins, and bind polypeptide ligands, mainly growth factors. Recent progress has been made towards an understanding of molecular mechanisms by which RTKs are activated by ligand binding. In this review, we discuss mainly about the mechanism of activation by which the epidermal growth factor (EGF/ErbB) receptor family, based upon recent structural and functional studies, and also discuss about other RTKs such as receptors for insulin and nerve growth factor.
Type of Paper: Review
Title: Unlocking Doors without Keys: Activation of Signaling Pathways by Truncated Intracellular Receptor Tyrosine Kinases
Authors: Belén Mezquita 1,2, Pau Mezquita 2, Montserrat Pau 1, Jovita Mezquita 1 and Cristóbal Mezquita 1,*
Affiliations: 1 Laboratori de Genètica Molecular, Departament de Ciències Fisiològiques I, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain
2 Department de Ciències Bàsiques, Facultat de Medicina i Ciències de la Salut, Universitat Internacional de Catalunya, Sant Cugat del Vallès, Spain; * E-Mail: email@example.com
Abstract: VEGFs are a family of growth factors that bind to tyrosine kinase receptors, VEGFR1 and VEGFR2, to activate a number of intracellular signaling pathways both in endothelial and cancer cells. We have characterized alternative transcripts of the VEGF receptor tyrosine kinase VEGFR1/flt1 in normal and cancer cells. These transcripts arise from intronic transcription start sites within the Flt1 gene. The new isoforms just contain portions of the intracellular tyrosine kinase domains and the C-terminal tail of the receptor. One of these transcripts is the main isoform of Flt1 expressed in MDA-MB-231 breast cancer cells. In these cells, the intracellular isoform activates Src and promotes cell invasion. The expression of this isoform is upregulated by Notch-1 and Notch-3 signaling pathways and downregulated by miR-200c and retinoic acid. Both, activation of Src and downregulation by retinoic acid, have been reported in other intracellular members of the Fms/Kit/PDGFR family of tyrosine kinases, such as the truncated intracellular isoform of c-kit. Truncated-kit has the same domains than the intracellular isoforms of Flt1, and both are preferentially expressed in cancer cells and sperm. An interesting possibility is that these proteins, through activation of Src, could be involved in the dynamic equilibrium between cancer non-stem and cancer stem cells.
Last update: 12 August 2013