2002
DOI: 10.1038/sj.cdd.4401108
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Cycling at the interface between neurodevelopment and neurodegeneration

Abstract: The discovery of cell cycle regulators has directed cell research into uncharted territory. In dividing cells, cell cycle-associated protein kinases, which are referred to as cyclin-dependent-kinases (Cdks), regulate proliferation, differentiation, senescence and apoptosis. In contrast, all Cdks in post-mitotic neurons, with the notable exception of Cdk5, are silenced. Surprisingly, misregulation of Cdks occurs in neurons in a wide diversity of neurological disorders, including Alzheimer's disease, Parkinson's… Show more

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Cited by 141 publications
(118 citation statements)
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References 105 publications
(170 reference statements)
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“…30 As shown in Figure 3, no significant changes were observed in the levels of cyclin D1 in cortical neurons treated with the peptides when compared to control cells. However, the subcellular distribution of this activator was altered from a more disperse nuclear/perinuclear pattern in control cells (Fig.…”
Section: Resultsmentioning
confidence: 80%
“…30 As shown in Figure 3, no significant changes were observed in the levels of cyclin D1 in cortical neurons treated with the peptides when compared to control cells. However, the subcellular distribution of this activator was altered from a more disperse nuclear/perinuclear pattern in control cells (Fig.…”
Section: Resultsmentioning
confidence: 80%
“…Moreover, activation of Cdks can be triggered in brain neurons after cerebral ischemia or kainate-induced excitotoxicity as well as in cultured neurons after treatment with DNAdamaging agents, deprivation of toxic factors, or ␤-amyloid peptide (Park et al 1997a(Park et al ,b, 1998a(Park et al ,b, 2000Copani et al, 1999;Stefanis et al, 1999;Osuga et al, 2000;Ino and Chiba, 2001;Katchanov et al, 2001). Under such in vivo and in vitro conditions, neuronal death can be rescued by the use of Cdk inhibitors or dominant negative forms of the kinases (Park et al 1997a(Park et al ,b, 1998a(Park et al ,b, 2000Copani et al, 1999;Stefanis et al, 1999;Osuga et al, 2000;Ino and Chiba, 2001;Katchanov et al, 2001), demonstrating the central role of Cdks in the neuronal apoptotic mechanism (for review, see Nguyen et al, 2002b).…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, mislocalization and deregulation of Cdk5 activity by association with p25, a toxic calpain-truncated form of p35, also participate in the pathogenesis of Alzheimer's disease and ALS (Patrick et al, 1999;Lee et al, 2000;Nguyen et al, 2001a). These data provided compelling evidence that alterations in the activities of Cdks can be noxious to neurons (for review, see Nguyen et al, 2002b).…”
Section: Introductionmentioning
confidence: 94%
“…Importantly, mutated Mfn2 that is not targeted to mitochondria does not impede the cell cycle control function, suggesting that Mfn2 control of cell cycle is fusion independent and Mfn2 function as a signaling GTPase [106]. There is compelling evidence that after induction of cell death, postmitotic neurons re-enter the cell cycle at G1-S and the deregulation of cell cycle proteins participate in cell death (for a detailed review see [109][110][111][112]). For example, DNA damage induced cell death triggers post-mitotic neurons to undergo S phase reentry, and inhibition of the cell cycle machinery can protect neurons against DNA damage [113][114][115][116].…”
Section: The Role Of Mitochondrial Fusion In Cell Death: Mfn1 and Mfnmentioning
confidence: 99%