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Titlebook: Control of Gene Expression by Catecholamines and the Renin-Angiotensin System; Heinz Rupp,Bernard Maisch Book 2000 Springer Science+Busine

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51#
發(fā)表于 2025-3-30 11:32:07 | 只看該作者
Angiotensin receptor II is present in dopaminergic cell line of rat substantia nigra and it is down ome (150 μM), a metabolite of the dopamine oxidative pathway, was found to down regu-late the expression of angiotensin receptor mRNA in RCSN3 cells by 83% (p < 0.05). (Mol Cell Biochem .: 131–134, 2000)
52#
發(fā)表于 2025-3-30 12:55:01 | 只看該作者
Control of cardiomyocyte gene expression as drug targeteuro-endocrine activation results in disordered influences of angiotensin II and catecholamines on gene expression. To assess whether angiotensin II type 1 receptor inhibition can also counteract a raised sympathetic nervous system activity, spontaneously hypertensive rats fed a hypercaloric diet we
53#
發(fā)表于 2025-3-30 19:23:51 | 只看該作者
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發(fā)表于 2025-3-30 21:31:38 | 只看該作者
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發(fā)表于 2025-3-31 01:18:26 | 只看該作者
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發(fā)表于 2025-3-31 05:41:39 | 只看該作者
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發(fā)表于 2025-3-31 10:37:43 | 只看該作者
58#
發(fā)表于 2025-3-31 14:31:30 | 只看該作者
Zum Transfer des Erarbeiteten in die Praxis, and alter gene expression. This review discusses a synthetic single-stranded palindromic oligonucleotide, which self-hybridizes to form a duplex/hairpin and competes with cAMP response element (CRE) enhancers for binding transcription factors. This oligonucleotide inhibits CRE- and Ap- 1-directed g
59#
發(fā)表于 2025-3-31 19:53:06 | 只看該作者
https://doi.org/10.1007/978-3-658-42882-2uating pro-apoptotic actions of chemotherapeutic agents or programmed cell death as a result of massive nitric oxide (NO) generation. Expression of Cox-2 was achieved by treatment of cells with lipopolysaccharide/interferon-γ or nontoxic doses of NO releasing agents. We reasoned E-type prostanoid fo
60#
發(fā)表于 2025-4-1 00:19:49 | 只看該作者
https://doi.org/10.1007/978-3-658-42934-8nd systemic IL-10 release in response to acute stress reactions in the absence of any systemic inflammation. . and . studies in experimental models suggest that catecholamines induce IL-10 release via a cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) dependent pathway. Here we studied pat
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