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B- and T-cell-specific inactivation of thioredoxin reductase 2 does not impair lymphocyte development and maintenance.

Biol. Chem. 388, 1083-1090 (2007)
DOI
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
Thioredoxin reductases (Txnrds) are a group of selenoenzymes participating in cellular redox regulation. Three Txnrd isoforms are known, each of which exhibits distinct cellular localisation and tissue-specific expression pattern. Txnrd1 is found in the cytoplasm, expression of Txnrd2 is restricted to mitochondria and Txnrd3 shows testis-specific expression. Recently, it was shown that Txnrd2 strongly affects the development of blood cells, since mouse embryos deficient for Txnrd2 are severely anaemic, show increased apoptosis in foetal liver and possess haematopoietic liver stem cells of reduced capacity to proliferate in vitro. However, because Txnrd2-deficient mice die at embryonic day 13.5, it was not known how this enzyme affects blood cell function in the adult animal. In the present study we show that conditional Txnrd2 knockouts generated using CD4- and CD19Cre transgenic mice lack Txnrd2 expression in CD4-- and CD19-positive T- and B-lymphocytes, respectively. However, the development and differentiation of both cell types in thymus and bone marrow was not significantly impaired. In addition, B-cell proliferation and activation in response to CD40 and IL-4 was unaltered in Txnrd2-deficient B-cells.
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Publication type Article: Journal article
Document type Scientific Article
Keywords CD4-Cre; CD19-Cre; conditional knockout; lymphocyte; selenoprotein
Language english
Publication Year 2007
HGF-reported in Year 2007
ISSN (print) / ISBN 1431-6730
e-ISSN 1437-4315
Quellenangaben Volume: 388, Issue: 10, Pages: 1083-1090 Article Number: , Supplement: ,
Publisher de Gruyter
Reviewing status Peer reviewed
POF-Topic(s) 30203 - Molecular Targets and Therapies
30202 - Environmental Health
Research field(s) Immune Response and Infection
Genetics and Epidemiology
PSP Element(s) G-501500-003
G-500900-001
Scopus ID 35348817982
Erfassungsdatum 2007-11-09