PuSH - Publication Server of Helmholtz Zentrum München

Conrad, M.

Transgenic mouse models for the vital selenoenzymes cytosolic thioredoxin reductase, mitochondrial thioredoxin reductase and glutathione peroxidase 4.

Biochim. Biophys. Acta-Gen. Subj. 1790, 1575-1585 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Selenium, as an integral part of selenoproteins, is essential for mammals. Unequivocal evidence had been provided more than a decade ago when it was proven that mice incapable of producing any of the 24 selenoproteins failed to develop beyond the gastrulation stage (E6.5). Since then, more specific attempts have been made to unmask novel and essential functions of individual selenoproteins in mice. Genetic disruption of glutathione peroxidase 4 (GPx4; also referred to as phospholipid hydroperoxide glutathione peroxidase, PHGPx) in mice showed for the first time that a specific selenoenzyme is in fact required for early embryonic development. Later on, systemic ablation of cytosolic thioredoxin reductase (Txnrd1) or mitochondrial thioredoxin reductase (Txnrd2) yielded embryonic lethal phenotypes. Beside those three, no other selenoproteins have been found being indispensable for murine development so far. This review aims at summarizing mainly the in vivo findings on these important mammalian selenoenzymes, which have not only common attributes of being required for embryogenesis, but that they are also instrumental in the regulation of cellular redox metabolism.
Altmetric
Additional Metrics?
[➜Log in]
Edit extra informations Login
Publication type Article: Journal article
Document type Review
Corresponding Author
Keywords Apoptosis inducing factor (aif); cre/loxp; 12/15-lipoxygenase; Oxidative stress; phgpx; Redox regulation; Early embryonic lethality; Apoptosis-inducing factor; Carcinoma a431 cells; Transfer-rna gene; Mammalian thioredoxin; Oxidative stress; Targeted disr
ISSN (print) / ISBN 0304-4165
e-ISSN 1872-8006
Journal Biochimica et Biophysica Acta - General Subjects
Quellenangaben Volume: 1790, Issue: 11, Pages: 1575-1585 Article Number: , Supplement: ,
Publisher Elsevier
Publishing Place Amsterdam
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)