Special Issue "Transcriptional Regulation of Pro-Inflammatory Genes"
A special issue of Biomolecules (ISSN 2218-273X).
Deadline for manuscript submissions: closed (30 April 2015)
Cytokines, chemokines, their receptors, and other inflammatory mediators are essential for a proper immune response during infection. Yet, their increased expression is a hallmark of chronic inflammatory disorders, metabolic disorders, and many types of cancer, highlighting the need for stringent regulation of pro-inflammatory gene expression. The nuclear factor-κB (NFκB) family of transcription factors is a central coordinator of the pro-inflammatory gene expression.
While tremendous progress has been made in understanding the pathways and mechanisms leading to NFkB activation, many unanswered questions remain regarding the mechanisms responsible for selectivity and termination of NFκB responses, modulation of NFκB-dependent transcription by post-translational modification of NFκB subunits and their interactions with other transcription factors and regulators, and metabolic regulation of inflammatory gene expression.
This issue intends to present original research articles and up-to-date reviews about all aspects of the transcriptional regulation of inflammatory genes, with a special focus on the regulation of NFκB-dependent inflammatory genes in cancer and metabolic disorders.
We look forward to reading your contributions,
Prof. Dr. Ivana Vancurova
Manuscript Submission Information
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. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short 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 thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 650 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- cytokine receptors
- transcriptional regulation
- metabolic disorders
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: Chemokine transcriptional regulation in ovarian cancer
Authors: Bipradeb Singha and Ivana Vancurova
Affiliation: Department of Biological Sciences, St. John’s University, 8000 Utopia Parkway, New York, NY 11439, USA; E-Mail: email@example.com (I.V.)
Abstract: The increased expression of pro-inflammatory and pro-angiogenic chemokines contributes to ovarian cancer progression through the induction of tumor cell proliferation, survival, angiogenesis, and metastasis. The substantial potential of these chemokines to facilitate the progression and metastasis of ovarian cancer underscores the need for their stringent transcriptional regulation. In this Review, we highlight the key mechanisms that regulate the transcription of pro-inflammatory chemokines in ovarian cancer cells, and that have important roles in controlling ovarian cancer progression. We further discuss the potential mechanisms underlying the increased chemokine expression in drug resistance, along with our perspective for future studies.
Type of Paper: Review
Title: Chemokine Transcriptional Regulation: A Link to Islet Inflammation
Authors: Susan J. Burke and J. Jason Collier
Affiliation: Laboratory of Islet Biology and Inflammation, Pennington Biomedical Research Center, 6400 Perkins Rd, Baton Rouge, LA 70808, USA; E-Mail: Jason.Collier@pbrc.edu (J.C.)
Abstract: Enhanced expression of chemotactic cytokines (aka chemokines) within pancreatic islets contributes to islet inflammation via the recruitment and activation of various leukocyte populations, including macrophages, neutrophils, and T-lymphocytes. The powerful action of these chemokines to regulate islet inflammation is congruent with the need to keep them under precise transcriptional control. In this review, we highlight the key mechanisms that govern the transcription of genes encoding chemokine proteins in pancreatic islet β-cells, which includes emphasis on the NF-κB and STAT1 pathways. We further discuss the implications of increased chemokine expression during autoimmune-mediated and obesity-related development of diabetes.
Type of Paper: Review
Title: Splicing Regulation of Cytokines and Chemokines with Pro-Inflammatory Functions in Normal Conditions and in Disease: at the Interface of the Neuroendocrine and Immune Systems
Author: Matteo Ruggiu
Affiliation: St. John’s University Department of Biological Sciences, St. Albert Hall, Room 202 8000 Utopia Parkway, Queens, NY 11439, USA; E-Mail: firstname.lastname@example.org
Abstract: Alternative splicing plays a key role in posttranscriptional regulation of gene expression, allowing a single gene to encode multiple protein isoforms. As such, alternative splicing amplifies the coding capacity of the genome enormously, generates protein diversity and alters protein function. More than 90% of human genes undergo alternative splicing, and alternative splicing is especially prevalent in the nervous and immune systems, tissues where cells need to react swiftly and adapt to changes in the environment through carefully regulated mechanisms of cell differentiation, migration, targeting and activation. Given its prevalence and complexity, this highly regulated mode of gene expression is prone to be affected by disease. In the following review we look at how alternative splicing of cytokines and chemokines changes in different pathological conditions, from chronic inflammation to neurologic disorders. Switches in alternative splicing patterns can be very dynamic and can produce cytokines with distinct or antagonistic functions and localized to different subcellular compartments. We also discuss recent studies highlighting how alternative splicing provides a means of functional interaction between the immune and neuroendocrine systems by generating distinctive isoforms of regulatory molecules and by regulating expression of specific splicing factors during stress, cerebral ischemia and diabetes. This newly discovered link expands our understanding of the biology of immune and neuroendocrine cells, and has the potential to open new windows of opportunity for treatment of metabolic and neurodegenerative disorders.