Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.8 (FAST)
758 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development and functions of female reproductive tissues are regulated by the actions of two major sex steroid hormones, estrogen and progesterone. To investigate estrogen-dependent gene expression in the rat uterus, we studied the effect of ovariectomy with or without estrogen treatment on the uterine expression of 3000 genes using cDNA microarrays. Many genes were regulated by either treatment, but only few were reciprocally regulated by these contrasting treatments. The present study confirms previous findings and identifies several genes with expressions not previously known to be influenced by estrogen. These genes include follistatin-related protein, Thy-1 glycoprotein, alpha-fodrin, CD24, immediate early response 5, insulin-like growth factor-binding protein 2, growth response protein CL-6 (INSIG-1), ladinin1, class I major histocompatibility complex heavy chain, lactadherin, ezrin, and Fas-activated serine/threonine kinase. Because of their function as regulators of proliferation and apoptosis, CD24, insulin-like growth factor-binding protein 2, and Fas/Fas ligand were examined further by immunohistochemical expression and tissue localization analysis. Our analysis confirms a contrasting regulation of these gene products by ovariectomy and estrogen treatment. The present study identifies novel mediators of estrogen actions in the uterus and provides genome-wide expression data from which novel hypotheses regarding uterine function can be generated.
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PMID:Gene expression profiling of the effects of castration and estrogen treatment in the rat uterus. 1280 95

Exercise stimulates growth hormone (GH) release, but there are conflicting reports regarding the acute effects of exercise on circulating ghrelin and insulin-like growth factor (IGF) concentrations. This investigation examined (1) the effect of a single sprint on circulating GH, ghrelin and IGF concentrations as well as a marker of IGF-I bioactivity, and (2) whether the number of muscle actions performed during a sprint influences these responses. Seven healthy men completed 3 trials in a random order. In two exercise trials they performed a single 30-s sprint on a cycle ergometer against a resistance equivalent to either 7% (FAST) or 9% (SLOW) of their body mass. In the other they rested in the laboratory (CON). Blood samples were taken pre-, immediately post-, 10 and 30 min post-exercise, and at equivalent times in the CON trial. Total ghrelin concentrations declined after the sprint and were significantly lower after 30 min of recovery than they were pre-exercise (pre-exercise vs. 30 min; FAST, 0.62 (0.19) vs. 0.49 (0.16) microg/L, P<0.001; SLOW, 0.59 (0.15) vs. 0.47 (0.13) microg/L, P<0.001). GH concentrations increased in both exercise trials and were greater in the FAST than the SLOW trial. Serum concentrations of total IGF-I, free IGF-I, total IGF-II, and IGF-I bioactivity did not change after sprinting. In conclusion, sprint exercise suppresses total ghrelin concentrations and stimulates GH release but does not alter IGF concentrations or bioactivity.
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PMID:Brief, high intensity exercise alters serum ghrelin and growth hormone concentrations but not IGF-I, IGF-II or IGF-I bioactivity. 2047 80