NDLI: Overexpression of Batf induces an apoptotic defect and an associated lymphoproliferative disorder in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Logan, M. R. Jordan-Williams, K. L. Poston, S. Liao, J. Taparowsky, E. J.
Description	Country affiliation: United States Author Affiliation: Logan MR ( Department of Biological Sciences, College of Science, Purdue University, West Lafayette, IN 47907-2064, USA.)
Abstract	Activator protein-1 (AP-1) is a dimeric transcription factor composed of the Jun, Fos and Atf families of proteins. Batf is expressed in the immune system and participates in AP-1 dimers that modulate gene expression in response to a variety of stimuli. Transgenic (Tg) mice overexpressing human BATF in T cells were generated using the human CD2 promoter (CD2-HA (hemagglutinin antigen) - BATF). By 1 year of age, over 90% of the mice developed a lymphoproliferative disorder (LPD). The enlarged lymph nodes characteristic of this LPD contain a polyclonal accumulation of T cells with a CD4(+) bias, yet efforts to propagate these tumor cells in vitro demonstrate that they do not proliferate as well as wild-type CD4(+) T cells. Instead, the accumulation of these cells is likely due to an apoptotic defect as CD2-HA-BATF Tg T cells challenged by trophic factor withdrawal in vitro resist apoptosis and display a pro-survival pattern of Bcl-2 family protein expression. As elevated levels of Batf expression are a feature of lymphoid tumors in both humans and mice, these observations support the use of CD2-HA-BATF mice as a model for investigating the molecular details of apoptotic dysregulation in LPD.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2012.49
Journal	Cell Death and Disease
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2012-05-17
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Promoter Regions, Genetic Research Support, Non-u.s. Gov't Lymphoproliferative Disorders Mice, Inbred C57bl Antigens, Cd2 Mice, Transgenic Transcription Factor Ap-1 Metabolism Discipline Cell Biology Pathology T-lymphocytes Animals Basic-leucine Zipper Transcription Factors Caspase 3 Hemagglutinins Genetics Mice Proto-oncogene Proteins C-bcl-2 Apoptosis Disease Models, Animal
Content Type	Text
Resource Type	Article

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