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Identification of androgen response elements in the insulin-like growth factor I upstream promoter.
Testosterone stimulates the expression of IGF-I in cells and tissues that include prostate, muscle and muscle satellite cells, and the uterus. Here, the molecular mechanisms of this effect ofExpand
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Dependence of dexamethasone-induced Akt/FOXO1 signaling, upregulation of MAFbx, and protein catabolism upon the glucocorticoid receptor.
The muscle ubiquitin ligases MAFbx and MuRF1 are upregulated in and promote muscle atrophy. Upregulation of MAFbx and MuRF1 by glucocorticoids has been linked to activation of FOXO1 and FOXO3AExpand
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Protection against dexamethasone-induced muscle atrophy is related to modulation by testosterone of FOXO1 and PGC-1α.
Glucocorticoid-induced muscle atrophy results from muscle protein catabolism and reduced protein synthesis, associated with increased expression of two muscle-specific ubiquitin ligases (MAFbx andExpand
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Differential skeletal muscle gene expression after upper or lower motor neuron transection
Causes of disuse atrophy include loss of upper motor neurons, which occurs in spinal cord injury (SCI) or lower motor neurons (denervation). Whereas denervation quickly results in muscleExpand
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REDD1 is a major target of testosterone action in preventing dexamethasone-induced muscle loss.
Glucocorticoids are a well-recognized and common cause of muscle atrophy that can be prevented by testosterone. However, the molecular mechanisms underlying such protection have not been described.Expand
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Effects of nandrolone on denervation atrophy depend upon time after nerve transection
Anabolic steroids prevent disuse atrophy and reverse atrophy caused by glucocorticoids. To determine whether these beneficial effects extend to denervation atrophy, we tested whether nandroloneExpand
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Differential alterations in gene expression profiles contribute to time-dependent effects of nandrolone to prevent denervation atrophy
BackgroundAnabolic steroids, such as nandrolone, slow muscle atrophy, but the mechanisms responsible for this effect are largely unknown. Their effects on muscle size and gene expression depend uponExpand
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Nandrolone normalizes determinants of muscle mass and fiber type after spinal cord injury.
Spinal cord injury (SCI) results in atrophy of skeletal muscle and changes from slow oxidative to fast glycolytic fibers, which may reflect reduced levels of peroxisome proliferator-activatedExpand
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Nandrolone, an anabolic steroid, stabilizes Numb protein through inhibition of mdm2 in C2C12 myoblasts.
Nandrolone, an anabolic steroid, slows denervation atrophy of rat muscle, prevents denervation-induced nuclear accumulation of intracellular domain of the Notch receptor, and elevates expression ofExpand
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Nandrolone reduces activation of Notch signaling in denervated muscle associated with increased Numb expression.
Nandrolone, an anabolic steroid, slows denervation-atrophy in rat muscle. The molecular mechanisms responsible for this effect are not well understood. Androgens and anabolic steroids activate NotchExpand
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