A Sequel to the Tale of p25/Cdk5 in Neurodegeneration
نویسندگان
چکیده
p25/Cdk5 dysregulation may contribute to neurodegeneration. In this issue of Neuron, Kim et al. show that cdk5 inactivates HDAC-1, leading to cell cycle deregulation and DNA damage accumulation. This study provides further insights into the function of p25/Cdk5 in neurons and points to HDAC-1 as a target for therapeutic interventions.
منابع مشابه
Specific inhibition of p25/Cdk5 activity by the Cdk5 inhibitory peptide reduces neurodegeneration in vivo.
The aberrant hyperactivation of Cyclin-dependent kinase 5 (Cdk5), by the production of its truncated activator p25, results in the formation of hyperphosphorylated tau, neuroinflammation, amyloid deposition, and neuronal death in vitro and in vivo. Mechanistically, this occurs as a result of a neurotoxic insult that invokes the intracellular elevation of calcium to activate calpain, which cleav...
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ورودعنوان ژورنال:
- Neuron
دوره 60 شماره
صفحات -
تاریخ انتشار 2008