PuSH - Publikationsserver des Helmholtz Zentrums München

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)
Verlagsversion PDF DOI
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.
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Zeitschrift PLoS ONE
Quellenangaben Band: 8, Heft: 11, Seiten: , Artikelnummer: e81833 Supplement: ,
Verlag Public Library of Science (PLoS)
Verlagsort Lawrence, Kan.
Begutachtungsstatus Peer reviewed