proteinkinasecanditsinvolvementinpathophysiologicdisorders(编辑修改稿)

proteinkinasecanditsinvolvementinpathophysiologicdisorders(编辑修改稿)内容摘要：

ation. Decreases in intracellular ATP also lead to ROS production, contributing to cPKC activation. Stroke. 20xx。 36:27812790. Email: cPKC may potentiate NMDAR function via Src tyrosine kinases. This feedback mediates increases in intracellular calcium, leading to mitochondrial dysfunction, ROS formation, and cell death. Stroke. 20xx。 36:27812790. Email: nPKC in Reperfusion Injury nPKC is specifically upregulated and rapidly activated in response to reperfusion induced intracellular signaling. (J Cereb Blood Flow Metab. 20xx。 20:93–102.) nPKC levels are increased in the perifocal region during reperfusion, suggesting a role for this enzyme in mediating delayedinjury processes. (J Neurosci. 1996。 16: 6236–6245.) Delivery of the PKCspecific inhibitor peptide V11 significantly reduced ischemic injury delivered in the reperfusion period, but not before ischemia. (J Neurosci. 20xx。 24:6880–6888.) Email: Reperfusion injury contributes to detrimental cell signaling, in part via release of glutamate and free radicals from the ischemic core and the recruitment of inflammatory mediators. Stroke. 20xx。 36:27812790. Email:  The effects of PLC, as well as rises in ROS, activate nPKC. Stroke. 20xx。 36:27812790. Email: Release of cytochrome C promotes apoptosis through the activation of caspases and subsequent DNA damage events in the nucleus. Stroke. 20xx。 36:27812790. Email:  Studies of PKC Activity and Function in In Vivo Cerebral Ischemia Models Stroke. 20xx。 36:27812790. Email: Stroke. 20xx。 36:27812790. Email: PKC amp。 Cerebral Hypoxic Preconditioning PKC Involved in Pathophysiologic Disorders Email: Hypoxic Preconditioning When exposed to sublethal ischemic episode, the brain enacts endogenous neuroprotective mechanisms to induce tolerance, rendering it protected against a subsequent lethal transient ischemic attack.  early preconditioning  delayed preconditioning The activation or translocation of PKC in the central nervous system may play a key role in mediating both early and delayed preconditioning. Email: Email: Email: Email: Gene transcription, Protein synthesis P P PKCβⅡ , γ, ε mGluR Early HPC Delayed HPC Hypoxia NMDAR AR PLC α γ β PIP2 IP3 DAG Ca2+ ER K+ATP channel ERK JNK p38 P P P P P P MAPK α, βI, βII, γ δ, ε, ε, ζ δ, η/λ PKC TykR Unknown ? Glutamate Adenosine Po2 MSK, RSK, Ng… P P P Known glucose ATP Email: PKC amp。 Alzheimer’s disease PKC Involved in Pathophysiologic Disorders Email: Alzheimer’s disease (AD) Clinical features: impairment in short term memory. Pathological characteristics: senile plaques, neurofibrillary tangles and neuronal loss, involving cholinergic pathways. In AD brain, cPKC and nPKC are decreased in the temporal cortex, both as levels and activities. (J Neurochem 1996。 67: 317–23) In peripheral Tcells from early AD patients, A increase nPKC expression, while in severe AD patients A induces nPKC a。