Journal of Cell Death
Synopsis: An open access, peer reviewed electronic journal that covers natural and pathological aspects of all types of cell death.
Indexing: Indexed by OAIster. Pubmed indexing for NIH-funded research.
Processing time: Decision in 2 weeks for 90% of papers.
Visibility: Most popular article read 300+ times.
About this journal
Aims and scope:
Journal of Cell Death is an open access, peer reviewed journal which covers research into all types and aspects of cell death, both natural and pathological, and at both the basic and applied levels. This includes the causes, cellular components, pathways, mediators and processes involved, as well as biochemistry, morphological changes, genetics and function.
Of particular interest are the implications necrotic and apoptotic processes have for disease and treatment together with the phagocytic mechanisms responsible for the disposal of cellular corpses. Related topics such as autophagocytosis are also included.
Indexing:
This journal is indexed by:
- OAIster
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.
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:
Read the Editor in Chief's latest call for papers here.
Submission types accepted:
Submissions of the following types of manuscripts are accepted:
- 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.
- Commentaries: focused and opinionated articles on any subject within the journal's scope. These articles are usually related to a contemporary issue.
- 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 ,
- Provide online-early rapid publication if your paper prior to typesetting.
What other authors have said:
Libertas Academica actively requests, receives and acts upon feedback from authors, readers and editorial boards. Here's what some recent authors have said about us:
"Within a couple of days the reviewers had been procured and the manuscript was out."
"The communication between your staff and me has been terrific. Whenever progress is made with the manuscript, I receive notice. Quite honestly, I've never had such complete communication with a journal."
"LA is different, and hopefully represents a kind of scientific publication machinery that removes the hurdles from free flow of scientific thought."
Article processing fees:
All submissions to this journal are subject to an article processing fee if they are accepted for publication. Article processing fees are used to fund the processing of your paper and development of the journal. Article processing fees are the only compulsory charge you will face and do not vary according to word count, page count, colour figures or any other factor. There is no additional charge for the author(s) to make any use of their article and no charge to readers to access it.
Full fee waivers are available for authors working in undeveloped nations and partial discounts of 20-50% are available to authors in other nations. Authors must be able to verifiably demonstrate their suitability for a discount or waiver. Availability of waivers and discounts is subject to monthly availability and is given at the publisher's discretion. Waivers and discounts must be applied for prior to submission. Neither are available after submission.
Register as a peer reviewer:
Do you wish to register as a peer reviewer? Or are you already a registered peer reviewer but you need to update your contact details? To register or update your details visit the peer reviewer registration form.
Applicants must be able to demonstrate at least five years of continuous experience in the journal's subject area including at least two in the previous 24 months.
The Editor in Chief has issued a new call for papers. Read it here.
Journal newsletter sent to subscribers in week 25, 2009. Register to receive future newsletters.
Peer reviewers are sought. Click here to apply or to update your details.
Read an interview with the Editor in Chief, and the announcement of the launch of the journal.
Check the Publisher's Blog for recent news
RTKN2 Induces NF-KappaB Dependent Resistance to Intrinsic Apoptosis in HEK Cells and Regulates BCL-2 Genes in Human CD4+ Lymphocytes
Fiona M Collier1,4, Andrea Loving1, Adele J Baker2, Janet McLeod3, Ken Walder4 and Mark A Kirkland1
1Barwon Biomedical Research, Geelong Hospital, Barwon Health, Ryrie St, Geelong, Victoria, 3227, Australia. 2Department of Malignant Haematology and Stem Cell Transplantation, The Alfred Hospital, Melbourne, Victoria, 3181, Australia. 3School of Medicine, Deakin University, Waurn Ponds, Victoria, 3217, Australia. 4Metabolic Research Unit, School of Medicine and Institute for Technology Research and Innovation, Deakin University, Waurn Ponds, Victoria, 3217, Australia.
Abstract
The gene for Rhotekin 2 (RTKN2) was originally identified in a promyelocytic cell line resistant to oxysterol-induced apoptosis. It is differentially expressed in freshly isolated CD4+ T-cells compared with other hematopoietic cells and is down-regulated following activation of the T-cell receptor. However, very little is known about the function of RTKN2 other than its homology to Rho-GTPase effector, rhotekin, and the possibility that they may have similar roles. Here we show that stable expression of RTKN2 in HEK cells enhanced survival in response to intrinsic apoptotic agents; 25-hydroxy cholesterol and camptothecin, but not the extrinsic agent, TNFα. Inhibitors of NF-KappaB, but not MAPK, reversed the resistance and mitochondrial pro-apoptotic genes, Bax and Bim, were down regulated. In these cells, there was no evidence of RTKN2 binding to the GTPases, RhoA or Rac2. Consistent with the role of RTKN2 in HEK over-expressing cells, suppression of RTKN2 in primary human CD4+ T-cells reduced viability and increased sensitivity to 25-OHC. The expression of the pro-apoptotic genes, Bax and Bim were increased while BCL-2 was decreased. In both cell models RTKN2 played a role in the process of intrinsic apoptosis and this was dependent on either NF-KappaB signaling or expression of downstream BCL-2 genes. As RTKN2 is a highly expressed in CD4+ T-cells it may play a role as a key signaling switch for regulation of genes involved in T-cell survival.
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Introductory Editorial (Journal of Cell Death)
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