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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.

Processing time: Decision in 2 weeks for 90% of papers.

Visibility: Most popular article read 300+ times.

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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. 



 
 
 


Increased Mitochondrial Activity in Anthrax-Induced Cell Death

Authors: Chi Li
Publication Date: 04 Sep 2009
Journal of Cell Death 2009:2 41-44

Chi Li

Molecular Targets Group, James Graham Brown Cancer Center, Department of Pharmacology and Toxicology, University of Louisville, KY 40202.

Abstract

Pathogenesis of anthrax lethal toxin (LT) is attributed to its ability to cause death of infected cells. New work has demonstrated that increase of mitochondrial F1F0 ATPase activity and subsequent depletion of cellular ATP level are critical early events during LT-induced cell death.

Categories: Cell death


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