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Publication : Profiling metabolic remodeling in PP2Acα deficiency and chronic pressure overload mouse hearts.

First Author  Dong D Year  2015
Journal  FEBS Lett Volume  589
Issue  23 Pages  3631-9
PubMed ID  26497085 Mgi Jnum  J:227856
Mgi Id  MGI:5703685 Doi  10.1016/j.febslet.2015.10.016
Citation  Dong D, et al. (2015) Profiling metabolic remodeling in PP2Acalpha deficiency and chronic pressure overload mouse hearts. FEBS Lett 589(23):3631-9
abstractText  Our understanding of how metabolic switches occur in the failing heart is still limited. Here, we report the emblematic pattern of metabolic alternations in two different mouse models. PP2Acalpha deficient hearts exhibited a dramatic decrease in the levels of mRNA encoding for transporters and enzymes involved in glucose utilization, which compensated by higher expression levels of genes controlling fatty acid utilization. These features were partly reproduced in cultured PP2Acalpha KD cardiomyocytes. Equivalently, a decrease in the expression of most of the transporters and enzymes controlling both glucose and fatty acid metabolism were observed in TAC model.
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