proteinkinasecanditsinvolvementinpathophysiologicdisorders-文庫吧
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【正文】 dances Among Effects Using Peptide Translocation inhibitors and Activators of Specific PKC Isozymes Current Pharmaceutical Design 20xx。 11: 549559 Email: PKC amp。 Cerebral Ischemia/ Reperfusion Injury PKC Involved in Pathophysiologic Disorders Email: ?Ischemic core ? Distal to an occluded artery, undergoes rapid, anoxic cell death within minutes. ? Irreversible processes: mitochondrial collapse, rapid energy depletion, and ion pump failure result in large increases in intracellular calcium, extracellular potassium, and edematous cell swelling, characteristic of necrotic cell death ?Ischemic penumbra ? Metabolism and intracellular signaling cascades are maintained partly by hypoperfusion from a diminished collateral blood supply. ? Affected by multiple stresses: regional glutamate, potassium diffusion and periinfarct depolarizations emanating from the ischemic core. Email: Email: ?Ischemic Tolerance: Role of nPKC? ? Sustained activation of nPKC? after OGD. (Neuropharmacology 20xx。 47: 136 –145) ? Delivery of an nPKC? inhibitor peptide abates NMDAinduced preconditioning in cell culture and isolated hippocampal slice models. (J Neurosci. 20xx。23:384 –391) ? Delivery of an nPKC? specific activator peptide before OGD reduces damage, in pure neuronal and mixed neuronal/astrocyte cultures. (Neuropharmacology. 20xx。 47:136 –145) ? The protective effect of the nPKC? activator was lost when delivered after OGD in these models. (Neuropharmacology. 20xx。 47:136 –145) Email: ?Preconditioning stimuli, including hypoxia, lead to a decrease in cellular ATP stores and the subsequent generation of adenosine, A1/A3 adenosine receptors (ARs) activate PLC via Gproteins. Stroke. 20xx。36:27812790. Email: ?PLC causes membrane damage, increasing DAG production, which activates nPKC?. Stroke. 20xx。36:27812790. Email: ? nPKC? induce opening of K (ATP) channels in the mitochondria, maintain ATP production and reduce generation of ROS. nPKC? leads to activation of ERK, which is involved in antiapoptotic signaling and cell survival. Stroke. 20xx。36:27812790. Email: ?Ischemia and the Role of Neuronal cPKC? cPKC? may play a deleterious role during early ischemic injury, but might play an opposite role after reperfusion. ? The use of PKC knockout mice suggest that cPKC? may play a detrimental role during cerebral ischemic injury. (ILAR J. 20xx。44:105–109) ? cPKC? is activated specifically during reperfusion. (J Cereb Blood Flow Metab. 20xx。24:54–61) ? cPKC? knockout mice demonstrate worsened injury after a transient ischemia, suggesting cPKC? may mediate beneficial signaling processes during reperfusion injury. (J Cereb Blood Flow Metab. 20xx。20:343–349) Email: ?Ischemiainduced reduction in blood oxygen and glucose delivery to the brain causes reduction in cellular ATP levels, leading to deregulation of cellular ion pumps and loss of intracellular ion homeostasis. Stroke. 20xx。36:27812790. Email: ?Rising intracellular calcium, causes activation of phospholipase C (PLC), which increases cPKC? activ
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