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gi protein
Phospholipids such as PA and LPA have been observed to prevent prostaglandin-induced increases in adenylate cyclase activity in other cell types via their effects on such a pertussis toxin sensitive Gi protein.
      
These data suggest that Mg++-induced chemotaxis may be promoted through a Gi protein-coupled receptor pathway with a requirement for protein kinase C activity and protein tyrosine phosphorylation.
      
Treatment of neutrophils with pertussis toxin (PTX), a Gi protein inhibitor, caused only ~75% loss of nucleotide-induced Ca2+ mobilization indicating that nucleotides cause Ca2+ mobilization both through Gi-dependent and Gi-independent pathways.
      
Exposure of cells to pertussis toxin prior to MPP+ eliminated the anti-apoptotic effect of guanosine, indicating that this effect is dependent on a Gi protein-coupled receptor, most likely the putative guanosine receptor.
      
Activity of mastoparan decreased in the presence of C-terminal peptide 346-355 from the Gi protein αi2-subunit.
      
We have demonstrated that chimeras with a third cytoplasmic loop of D2 receptor couple to Gi protein in a pattern characteristic of D2 receptor.
      
Immunocytochemical studies of the Gi Protein mediated muscarinic receptor-adenylyl cyclase system
      
The Gi protein rapidly loses functional activity during very early myocardial ischemia.
      
In contrast to Gi protein, the function of Gs protein during this phase has not been evaluated.
      
It has become increasingly evident that Gi protein may play an important role in the cardioprotective effects of preconditioning.
      
When β-adrenoceptor densities are reduced in chronic myocardial ischemia, decreased in the amount and function of Gi protein and increased amount of Gs protein may play the role in preservation of the adenylate cyclase activity.
      
The carbachol response is blocked by pertussis toxin and is insensitive to the phosphodiesterase inhibitor, IBMX, suggesting an involvement of a Gi protein.
      
In cerebellar astrocytes S1P is able to mediate calcium signaling mainly through Gi protein coupled receptors, whereas in differentiated neurons it failed to evoke any calcium signaling, despite acting both extracellularly and intracellularly.
      
Ischemic preconditioning is associated with activation of myocyte Gi protein-coupled receptors such as adenosine and acetylcholine, activation of PKC, production of nitric oxide, and, eventually, opening of ATP-sensitive potassium (KATP) channels.
      
Our results show that deleting valine-125 and cysteine-126 in gI decreases plaque size and reduces virulence in mice to the same degree as deleting the gI protein.
      
Activation of Gi protein with the muscarinic receptor agonist carbachol protected against -ARstimulated apoptosis.
      
A causal connection between a Gi protein and adenylyl cyclase, as is found in somatic cells, has not yet been demonstrated in spermatozoa.
      
Conversely, pertussis toxin which modifies Gi protein stimulates Myf4 gene expression.
      
Effect of PKC and Gi protein signaling pathways on cAMP production in gallbladder epithelial cells.
      
Higher concentrations of GTP s reversed the maximum stimulation of cAMP, presumably through progressive activation of Gi protein.
      
 

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