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Gewies, A. ; Castineiras-Vilarino, M.* ; Ferch, U.* ; Jährling, N.* ; Heinrich, K.* ; Hoeckendorf, U.* ; Przemeck, G.K.H. ; Munding, M. ; Groß, O.* ; Schroeder, T. ; Horsch, M. ; Karran, E.L.* ; Majid, A.* ; Antonowicz, S.* ; Beckers, J. ; Hrabě de Angelis, M. ; Dodt, H.U.* ; Peschel, C.* ; Förster, I.* ; Dyer, M.J.S.* ; Ruland, J,

Prdm6 is essential for cardiovascular development in vivo.

PLoS ONE 8:e81833 (2013)
Publ. Version/Full Text PDF DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Members of the PRDM protein family have been shown to play important roles during embryonic development. Previous in vitro and in situ analyses indicated a function of Prdm6 in cells of the vascular system. To reveal physiological functions of Prdm6, we generated conditional Prdm6-deficient mice. Complete deletion of Prdm6 results in embryonic lethality due to cardiovascular defects associated with aberrations in vascular patterning. However, smooth muscle cells could be regularly differentiated from Prdm6-deficient embryonic stem cells and vascular smooth muscle cells were present and proliferated normally in Prdm6-deficient embryos. Conditional deletion of Prdm6 in the smooth muscle cell lineage using a SM22-Cre driver line resulted in perinatal lethality due to hemorrhage in the lungs. We thus identified Prdm6 as a factor that is essential for the physiological control of cardiovascular development.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Transcriptional Repressor Blimp-1 ; T-cell Homeostasis ; Vascular Development ; Smooth-muscle ; Endothelial-cells ; Breast-cancer ; Mice Lacking ; Yolk-sac ; Angiogenesis ; Gene
ISSN (print) / ISBN 1932-6203
Journal PLoS ONE
Quellenangaben Volume: 8, Issue: 11, Pages: , Article Number: e81833 Supplement: ,
Publisher Public Library of Science (PLoS)
Publishing Place Lawrence, Kan.
Non-patent literature Publications
Reviewing status Peer reviewed