Gene Regulation and Systems Biology
Synopsis: An open access, peer reviewed electronic journal that covers regulation of genes and proteins they encode and the broader field of systems biology.
Indexing: 7 major databases. Pubmed indexing for NIH-funded research.
Processing time: Decision in 2 weeks for 90% of papers.
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About this journal
Aims and scope:
Gene Regulation and Systems Biology is concerned with the regulation of genes and the proteins they encode and the relationship between gene regulation and the wider field of systems biology.
The regulation of genes and the proteins they encode is at the core of systems biology. Understanding the role of gene regulation in the context of the entire system as it relates to disease processes will aid therapeutic development. Therefore, combining our knowledge of gene expression and promoter control, improving gene and protein networks, and determining the role of signal transduction will enhance our ability to treat complex diseases.
Systems biology is concerned with the integration of different levels of information to understand how complex biological systems function. By studying the relationships and interactions between various parts of a biological system (including gene and protein networks involved in cell signaling) it may be possible to create an understandable model of the whole system. Mathematical, analytic, and particularly computer simulation and heuristics are used as research methods.
Editorial standards and procedures:
Submissions, excluding editorials, letters to the editor and dedications, will be peer reviewed by two reviewers. Reviewers are required to provide fair, balanced and constructive reports.
Under our Fairness in Peer Review Policy authors may appeal against reviewers' recommendations which are ill-founded, unobjective or unfair. Appeals are considered by the Editor in Chief or Associate Editor.
Papers are not sent to peer reviewers following submission of a revised manuscript. Editorial decisions on re-submitted papers are based on the author's response to the initial peer review report.
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This journal is indexed by the following services:
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National Institutes of Health Public Access Policy compliant:
As of April 7 2008, the US NIH Public Access Policy requires that all peer reviewed articles resulting from research carried out with NIH funding be deposited in the Pubmed Central archive.
If you are an NIH employee or grantee Libertas Academica will ensure that you comply with the policy by depositing your paper at Pubmed Central on your behalf.
Call for papers:
The Editor in Chief welcomes submissions. Submissions of the following types are invited:
- Original research articles.
- Reviews: comprehensive, authoritative, descriptions of any subject within the journal's scope. They may cover basic science and clinical reviews, ethics, pro/con debates, and equipment reviews.
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- Hypotheses: articles that present an original hypothesis backed solely by previously published results rather than any new evidence. They should outline significant progress in thinking that would also be testable.
- Letters to the Editor: these can be either a re-analysis of a previously published article, or a response to such a re-analysis from the authors of the original publication.
- Methodology articles: these discuss a new experimental method, test or procedure. The article must describe a demonstrable advance on what is currently available. The method needs to have been well tested and ideally, but not necessarily, used in a way that proves its value.
- Short reports: brief reports of data from original research.
- Meeting reports: a report pertaining to activity at a meeting or conference Articles published in this journal are immediately available without delay upon publication and enjoy substantial visibility.
- Case reports: reports of clinical cases that can be educational, describe a diagnostic or therapeutic dilemma, suggest an association, or present an important adverse reaction. Case reports must meet appropriate ethical standards.
All submissions are subject to prompt, objective and fair peer review in compliance with our Fairness in Peer Review Policy. Copyright in published articles remains with the author(s). Authors are continually informed of the progress of their paper and our staff are friendly and responsive.
One author recently wrote: "I would like to say that this is the most author-friendly editing process I have experienced in over 150 publications. Thank you most sincerely."
Criteria for publication:
Publication is dependent on peer reviewers' judgement of papers. Reviewers are asked to provide thoughtful and unbiased feedback to authors to ensure that the conclusions of papers are valid and manuscripts achieve reasonable standards of scholarliness and intelligibility.
Previous work in the field must be acknowledged and papers should read without unreasonable difficulty. Papers should fit comfortably within the scope of the journal.
Reviewers are asked to act in a fair, objective and constructive manner which maintains quality standards and helps authors to communicate their research. They are instructed that in areas of genuinely novel research issues may be raised which cannot immediately be resolved and that absolutely rigorous validation of data may therefore not be possible.
More information on the role of peer reviewers is available on the information for reviewers page. Where authors consider that reviewers have made recommendations which are unreasonable, unobjective or ill-founded they may appeal them to the Editor in Chief or Associate Editor under our Fairness in Peer Review Policy.
Articles submitted to other journals:
We are willing to consider papers which have been peer reviewed by other journals but not accepted for publication.
Services for authors:
Prior to peer review of your paper we can:
- Have your paper's reference style revised to meet our requirements,
- Have your paper's English revised by specialist English-speaking technical editors.
After peer review of your paper we can:
- Have your paper revised in accordance with peer reviewer's recommendations and have a summary of responses to the reviewers created by our specialist external substantive editors,
- Provide bound reprints of your article in colour or black and white ,
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Read an interview with the Editor in Chief.
Preclinical Assessment of wt GNE Gene Plasmid for Management of Hereditary Inclusion Body Myopathy 2 (HIBM2)
Chris Jay1, Gregory Nemunaitis2,5, John Nemunaitis2, Neil Senzer2, Stephan Hinderlich3, Daniel Darvish4, Julie Ogden2, John Eager1, Alex Tong1,6 and Phillip B Maples1
1Gradalis, Inc., Dallas, TX. 2Mary Crowley Cancer Research Centers, Dallas, TX. 3University of Applied Sciences Berlin, Department of Life Sciences and Technology, Germany. 4HIBM Research Group, Encino, CA. 5MetroHealth Medical Center, Cleveland, OH. 6Sammons Cancer Center, Baylor University Medical Center, Dallas, TX.
Abstract
Hereditary Inclusion Body Myopathy (HIBM2) is a chronic progressive skeletal muscle wasting disorder which generally leads to complete disability before the age of 50 years. There is currently no effective therapeutic treatment for HIBM2. Development of this disease is related to expression in family members of an autosomal recessive mutation of the GNE gene, which encodes the bifunctional enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK). This is the rate limiting bifunctional enzyme that catalyzes the first 2 steps of sialic acid biosynthesis. Decreased sialic acid production, consequently leads to decreased sialyation of a variety of glycoproteins including the critical muscle protein alpha-dystroglycan (α-DG). This in turn severely cripples muscle function and leads to the onset of the syndrome. We hypothesize that replacing the mutated GNE gene with the wildtype gene may restore functional capacity of GNE/MNK and therefore production of sialic acid, allowing for improvement in muscle function and/or delay in rate of muscle deterioration. We have constructed three GNE gene/CMV promoter plasmids (encoding the wildtype, HIBM2, and Sialuria forms of GNE) and demonstrated enhanced GNE gene activity following delivery to GNE-deficient CHO-Lec3 cells. GNE/MNK enzyme function was significantly increased and subsequent induction of sialic acid production was demonstrated after transfection into Lec3 cells with the wild type or R266Q mutant GNE vector. These data form the foundation for future preclinical and clinical studies for GNE gene transfer to treat HIBM2 patients.
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