Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Zhu, Y; Pires, KM; Whitehead, KJ; Olsen, CD; Wayment, B; Zhang, YC; Bugger, H; Ilkun, O; Litwin, SE; Thomas, G; Kozma, SC; Abel, ED.
Mechanistic target of rapamycin (Mtor) is essential for murine embryonic heart development and growth.
PLoS One. 2013; 8(1): e54221-e54221. [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Autor/innen der Med Uni Graz:
Bugger Heiko Matthias

Dimensions Citations:

Plum Analytics:
Number of Figures: 4
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Mechanistic target of rapamycin (Mtor) is required for embryonic inner cell mass proliferation during early development. However, Mtor expression levels are very low in the mouse heart during embryogenesis. To determine if Mtor plays a role during mouse cardiac development, cardiomyocyte specific Mtor deletion was achieved using α myosin heavy chain (α-MHC) driven Cre recombinase. Initial mosaic expression of Cre between embryonic day (E) 10.5 and E11.5 eliminated a subset of cardiomyocytes with high Cre activity by apoptosis and reduced overall cardiac proliferative capacity. The remaining cardiomyocytes proliferated and expanded normally. However loss of 50% of cardiomyocytes defined a threshold that impairs the ability of the embryonic heart to sustain the embryo's circulatory requirements. As a result 92% of embryos with cardiomyocyte Mtor deficiency died by the end of gestation. Thus Mtor is required for survival and proliferation of cardiomyocytes in the developing heart.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Blotting, Western -
Embryonic Development - genetics
Embryonic Development - physiology
Female -
Heart - embryology
Mice -
Mice, Knockout -
TOR Serine-Threonine Kinases - genetics
TOR Serine-Threonine Kinases - metabolism

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