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What is the role of messenger RNA for the protein synthesis?
Statins also influence other antioxidant enzymes, such as thioredoxin 1 and HO-1. In human endothelial cells, atorvastatin stimulated NO synthesis and hence S-nitrosylation of thioredoxin 1, increasing its activity and reducing intracellular ROS, while rosuvastatin increased mRNA and protein expression of HO-1.
The synthesis of NO by eNOS requires the presence of a cofactor, BH4. When BH4 binds to eNOS, the enzyme is coupled. Degradation of BH4 by ROS, particularly ONOO leads to the uncoupling of the enzyme and hence the production of O instead of NO. In turn, O reacts with NO, producing ONOO and oxidizing BH4, leading to a vicious cycle of eNOS uncoupling. Akt: protein kinase B; AMPK: adenosine monophosphate-activated protein kinase; mRNA: messenger ribonucleic acid; BH4: tetrahydrobiopterin; Poly(A): polyadenylate; Cav-1: caveolin-1; eNOS: endothelial nitric oxide synthase; GTPCH-1: guanosine triphosphate cyclohydrolase; NO: nitric oxide; O: oxygen; O: superoxide; ONOO: peroxynitrite; P: phosphate; PI3K: phosphoinositide 3-kinase; PKA: protein kinase A; ROS: reactive oxygen species; Ser633: serine 633; Ser1177: serine 1177.
What Is The Role Of Dna During Transcription In Protein Synthesis
Statins’ redox effects have been assessed in individuals with hyperlipidemia, in whom they have various protective effects, including reduced ROS production and increased platelet NO synthesis, decreased urinary and platelet isoprostanes, diminished platelet Rac1 activation, inhibiting of serum and platelet Nox2, increasing adiponectin levels and thereby reducing gp91phox and Nox activity, raised serum vitamin E levels, and decreased DNA damage in hypercholesterolemic individuals with the C242T polymorphism of the p22phox gene, which is associated with risk for developing CAD.
Statins can stimulate antioxidant defenses. In-vitro treatment of human endothelial cells with atorvastatin increased expression of catalase and MnSOD following phosphorylation of Akt at Ser473. In tumor cells, fluvastatin increased mRNA and protein expression of MnSOD and caused a two-fold increase in MnSOD activity. These effects appear to be due to downregulation of DNA damage-binding protein 2 (DDB2), a negative regulator of MnSOD transcription. Fluvastatin also increased catalase activity and GSH concentrations. Increased GSH has also been observed in promyelocytic cells treated with rosuvastatin, and appears to result from upregulation of gamma-glutamylcysteine synthetase, the rate-limiting enzyme of GSH.
What Is the Role of RNA in Protein Synthesis? (with …
Binding to BH4 is essential for eNOS to synthesize NO. Degradation of this cofactor by ROS leads to uncoupling of the enzyme and production of O instead of NO, as mentioned previously (). De novo synthesis of BH4 requires the enzyme guanosine triphosphate cyclohydrolase (GTPCH), a limiting factor for its formation. In human endothelial cells, fluvastatin and cerivastatin significantly increased the expression of messenger ribonucleic acid (mRNA) of GTPCH and intracellular BH4 concentrations. These statins also increased eNOS transcription. In another study, atorvastatin, pravastatin or pitavastatin also increased eNOS expression through stimulation of protein kinase B (Akt) at Ser473, inhibiting endothelial senescence induced by oxidative stress.
Statins stimulate the synthesis of NO by eNOS and by preventing eNOS uncoupling, limit the formation of ROS. Akt: protein kinase B; AMPK: adenosine monophosphate-activated protein kinase; mRNA: messenger ribonucleic acid; BH4: tetrahydrobiopterin; eNOS: endothelial nitric oxide synthase; Poly(A): polyadenylate; Cav-1: caveolin-1; GTPCH-1: guanosine triphosphate cyclohydrolase; NO: nitric oxide; O: oxygen; P: phosphate; PI3K: phosphoinositide 3-kinase; PKA: protein kinase A; Poly(A): polyadenylate; ROS: reactive oxygen species; Ser633: serine 633; Ser1177: serine 1177.
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role in the process of protein synthesis
Oxidative stress is defined as an imbalance between the synthesis of reactive oxygen species and their elimination by antioxidant defense systems, with a prevailing pro-oxidant status that results in macromolecular damage and disruption of cellular redox signaling. Reactive oxygen species interfere with various processes that affect cardiac structure and function, contributing to the contractile dysfunction, myocardial hypertrophy and fibrosis observed in the pathophysiology of heart failure. By regulating several molecular pathways that control nicotinamide adenine dinucleotide phosphate oxidase and endothelial nitric oxide synthase activity, statins help restore redox homeostasis. These drugs also contribute to the control of inflammation and appear to have a protective role in various diseases. The results of observational studies and clinical trials with statins in heart failure have not been consensual.
[Solved] Roles of RNA in protein synthesis in eukaryotes
Based on the aforementioned studies, it is knownthat exosomes secreted from MSCs may result in cell-to-celltransfer of mRNA, miRNA and proteins (). However, the exact roles and mechanismsof MSC-produced exosomes in tumor biology remain largelyelusive.
to the site of protein synthesis is messenger RNA or mRNA in ..
It has recently been suggested that statins’ inhibition of Nox may be partly mediated by adiponectin, a protein synthesized by adipocytes. In hypercholesterolemic patients, increases in adiponectin levels following treatment with atorvastatin were associated with decreases in the soluble form of gp91phox, platelet ROS production and urinary isoprostanes. In-vitro treatment with adiponectin also inhibited p47phox translocation and soluble gp91phox cleavage, inhibiting Nox activation in platelets.
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