A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Wessells, R., Fitzgerald, E., Piazza, N., Ocorr, K., Morley, S., Davies, C., Lim, H.Y., Elmén, L., Hayes, M., Oldham, S., Bodmer, R. (2009). d4eBP acts downstream of both dTOR and dFoxo to modulate cardiac functional aging in Drosophila.  Aging Cell 8(5): 542--552. (Export to RIS)
FlyBase ID FBrf0209169
Publication Type Research paper
PubMed ID 19594484
PubMed Abstract dTOR (target of rapamycin) and dFoxo respond to changes in the nutritional environment to induce a broad range of responses in multiple tissue types. Both dTOR and dFoxo have been demonstrated to control the rate of age-related decline in cardiac function. Here, we show that the Eif4e-binding protein (d4eBP) is sufficient to protect long-term cardiac function against age-related decline and that up-regulation of dEif4e is sufficient to recapitulate the effects of high dTOR or insulin signaling. We also provide evidence that d4eBP acts tissue-autonomously and downstream of dTOR and dFoxo in the myocardium, where it enhances cardiac stress resistance and maintains normal heart rate and myogenic rhythm. Another effector of dTOR and insulin signaling, dS6K, may influence cardiac aging nonautonomously through its activity in the insulin-producing cells, possibly by regulating dilp2 expression. Thus, elevating d4eBP activity in cardiac tissue represents an effective organ-specific means for slowing or reversing cardiac functional changes brought about by normal aging.
DOI 10.1111/j.1474-9726.2009.00504.x
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Language of Publication English
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Publication Type Journal
Abbreviation Aging Cell
Title Aging Cell
Publication Year 2002-
ISBN/ISSN 1474-9718 1474-9728
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