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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.

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About this journal

ISSN: 1179-0660



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. 



 
 
 


RTKN2 Induces NF-KappaB Dependent Resistance to Intrinsic Apoptosis in HEK Cells and Regulates BCL-2 Genes in Human CD4+ Lymphocytes

Authors: Fiona M Collier, Andrea Loving, Adele J Baker, Janet McLeod, Ken Walder and Mark A Kirkland
Publication Date: 07 Sep 2009
Journal of Cell Death 2009:2 9-23

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.

Categories: Cell death


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