2014
DOI: 10.1007/s12031-014-0466-5
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CDK5 Contributes to Neuronal Apoptosis via Promoting MEF2D Phosphorylation in Rat Model of Intracerebral Hemorrhage

Abstract: Cyclin-dependent kinase-5 (CDK5), a serine/threonine kinase which can be activated by its neuron-specific activator p35, or its truncated form p25, plays an important role in a variety of neuronal events, including neuronal migration, synaptic transmission, and neuronal death. Accumulating evidence has shown that abnormal activation of CDK5 was a critical neuronal pro-death signal in central nervous system (CNS) diseases. However, it remains unclear how CDK5 functions upon neuronal apoptosis following intracer… Show more

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Cited by 31 publications
(31 citation statements)
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“…BrdU-labeled cells in p25 TG mice expressed cleaved caspase-3, which is a biomarker of apoptosis, suggesting that p25-expressing neurons trigger cell apoptosis in these proliferating NPCs. These findings are consistent with previous studies that showed a critical role of p25/CDK5 in regulating neuronal apoptosis [34, 35]. Moreover, in agreement with previous study [36], most BrdU-labeled cells differentiated into both neurons and astrocytes.…”
Section: Discussionsupporting
confidence: 93%
“…BrdU-labeled cells in p25 TG mice expressed cleaved caspase-3, which is a biomarker of apoptosis, suggesting that p25-expressing neurons trigger cell apoptosis in these proliferating NPCs. These findings are consistent with previous studies that showed a critical role of p25/CDK5 in regulating neuronal apoptosis [34, 35]. Moreover, in agreement with previous study [36], most BrdU-labeled cells differentiated into both neurons and astrocytes.…”
Section: Discussionsupporting
confidence: 93%
“…Cdk5 mediates TrkB and ERK1/2 phosphorylation, induces neuronal death and spine loss and affects motor and cognitive deficits [45][46][47][48][49]. Moreover, thrombin, a serine protease, could enhance Cdk5 kinase activity [50]. Our data showed that NM increased the expression of BDNF, NGF and NT3 in the ipsilateral hippocampus, contralateral and ipsilateral sensorimotor cortex and activated the TrkB/ ERK1/2-CREB signaling pathway, inhibited Cdk5 activity in the ipsilateral hippocampus and contralateral sensorimotor cortex, but did not influence the phosphorylation of JNK and p38 MAPK.…”
Section: Discussionmentioning
confidence: 99%
“…The abnormal enhancement in Cdk5 activity triggered by isoflurane exposure ultimately leads to the subsequent neuronal apoptosis and cognitive deficits through inactivating MEF2, a direct nuclear target of Cdk5, at a distinct serine of transactivation domain in the developing brain [117]. Cdk5 is conscientious for neurotoxicity-induced apoptosis due to the interactions with Transcription factor MEF2 [118]. Furthermore, Cdk5-mediated degradation of MEF2D is known to be mediated by chaperone induced autophagy.…”
Section: Cdk5 Involves In Neuronal Cell Apoptosismentioning
confidence: 99%