protein kinase g การใช้

• In H2S therapy immediately following an AMI, increased cGMP triggers an increase in protein kinase G ( PKG ) activity.
• A kinase of the nitric oxide cell signalling pathway, protein kinase G, phosphorylates a small heat shock protein, hsp20.
• In H 2 S therapy immediately following an AMI, increased cGMP triggers an increase in protein kinase G ( PKG ) activity.
• For example, PKG ( protein kinase G ) is a catalytic and one regulatory unit, with the regulatory units blocking the active sites of the catalytic units.
• In the vascular endothelium, cGMP activates cGMP kinase or PKG ( protein kinase G ), which is an enzyme that belongs to a type of serine / threonine-specific protein kinase.
• As a consequence of increased concentrations, ammonia activity in-vivo has been shown to induce swelling of astrocytes in the brain through increased production of Protein Kinase G-mediated ( PKG ) cytoskeletal modifications.
• "' cGMP-dependent protein kinase "'or "'Protein Kinase G ( PKG ) "'is a serine / threonine-specific protein kinase that is activated by sperm metabolism, cell division, and nucleic acid synthesis.
• It was found that 種O acts through the stimulation of the soluble guanylate cyclase, which is a heterodimeric enzyme with subsequent formation of cyclic-GMP . Cyclic-GMP activates protein kinase G, which causes reuptake of Ca 2 + and the opening of calcium-activated potassium channels.
• It was found that NO acts through the stimulation of the soluble guanylate cyclase, which is a heterodimeric enzyme with subsequent formation of cyclic-GMP . Cyclic-GMP activates protein kinase G, which causes reuptake of Ca 2 + and the opening of calcium-activated potassium channels.
• Guanylate cyclase produces cyclic guanosine monophosphate ( cGMP ) from guanosine triphosphate ( GTP ) . cGMP in turn activates cyclic nucleotide-dependent protein kinase G, which phosphorylates various proteins that play a role in decreasing intracellular calcium levels, leading to relaxation of the muscle cells and thus to dilation of blood vessels.
• Klf4 also mediates the vascular response to nitric oxide ( NO ) by activating the promoters of inducible nitric oxide synthase ( iNOS ) in endothelial cells and cGMP-dependent protein kinase 1? / protein kinase G 1? ( RhoA signalling pathways and RhoA activation are implicated in hypertension and increased vascular resistance which to some extent can be explained by this interaction with Klf4 and its effects on the response to NO . Klf5 has no effect on the PKG 1? promoter though the protein expression and nuclear localisation of Klf5 was similar to that of Klf4.