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gi-protein
Thus, in the experimental type 2 diabetes, disturbances in Gi-protein coupled signal cascades are primarily observed, through which hormones realize their inhibition of AC activity.
      
From these results, a scheme is proposed which, links the regulation of noradrenaline release by prejunctional α2-adrenoceptors and protein kinase C via an influence on a common inhibitory Gi-protein.
      
Expression of endothelin (ET)-1, a 21-amino acid peptide and major isoform of the endothelin peptide family, is produced by endothelial, vascular smooth muscle cells, and macrophages and acts through Gi-protein-coupled ETA and ETB receptors.
      
Several Gi-protein-coupled receptors normally expressed in islet β-cells inhibit insulin secretion on binding of their respective agonists.
      
Our results suggest that overexpression of a Gi-protein-coupled receptor in β-cells causes tonic inhibition of both insulin synthesis and secretion.
      
Here, we describe a novel reporter gene assay system for the investigation of Gi-protein coupled receptors in living cells.
      
Furthermore, the novel reporter system was successfully applied to the neuropeptide Y (NPY) rY5 receptor subtype, a Gi-protein coupled receptor.
      
This ACSM includes the signaling chain: receptor-tyrosine kinase → Gi-protein → phosphatidylinositol 3-kinase → protein kinase C-zeta → Gs-protein → adenylyl cyclase → protein kinase A.
      
Chronic β-adrenoceptor stimulation leads to desensitization of the myocardial adenylyl cyclase signalling pathway which includes β-adrenoceptor downregulation and upregulation of Gi-protein α-subunits.
      
Another possibility could be that chronic β-AR blocker treatment normalizes activity of Gi-protein and may thereby restore β-AR functional responsiveness.
      
Nociceptin/orphanin FQ (N/OFQ) is the endogenous 17 amino acid peptide ligand for the Gi-protein-coupled N/OFQ receptor (NOP).
      
In conclusion, ICaT facilitation - which, as previously reported, is modulated by the transient voltage-dependent relief of Gi-protein inhibitory tone - is further enhanced in a low-Na+ solution.
      
The first stimulus is compound 48/80, and its action is mediated probably by a Gi-protein, while the other is sodium fluoride, which unspecifically activates G-proteins.
      
Pretreatment of cells with pertussis toxin markedly inhibits the secretion, suggesting a possible function of a Gi-protein in the activation pathway.
      
The attenuated responses of the aging heart to catecholamines are explained on the basis of depressed adenylyl cyclase and increased Gi-protein contents since no changes in β-adrenoceptors or Gs-proteins were seen in the aged myocardium.
      
Northern blot analysis revealed that the signals for Gs- and Gi-protein mRNAs were augmented at this stage of heart failure.
      
Ca2+-repletion also decreased protein content for AC and β-AR kinase but augmented the changes in Gs- and Gi-protein functions.
      
Epidermal growth factor-mediated signaling of Gi-protein to activation of phospholipases in rat-cultured hepatocytes.
      
The Gi-protein content was determined by Western blot as described below.
      
 

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