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M. Stanciu and D. B. DeFranco, “Prolonged Nuclear Re- Tention of Activated Extracellular Signal-Regulated Pro- tein Kinase Promotes Cell Death Generated by Oxidative Toxicity or Proteasome Inhibition in a Neuronal Cell Line,” Journal of Biological Chemistry, Vol. 277, No. 6, 2002, pp. 4010-4017. doi:10.1074/jbc.M104479200

has been cited by the following article:

• TITLE: Mitogen-Activated Protein Kinase Pathways Following Traumatic Brain Injury

  AUTHORS: Naoki Otani, Hiroshi Nawashiro, Kimihiro Nagatani, Satoru Takeuchi, Hiroaki Kobayashi, Katsuji Shima

  KEYWORDS: Traumatic Brain Injury, Mitogen-Activated Protein Kinase, Cell Signaling

  JOURNAL NAME: Neuroscience and Medicine, Vol.2 No.3, September 28, 2011

  ABSTRACT: The mechanisms underlying the secondary or delayed cell death in the hippocampus and cerebral hemisphere after traumatic brain injury (TBI) have been poorly understood. Recent data suggesting that TBI may have relationship with both an inflammatory and a neurodegenerative factors are also presented. Mitogen-activated protein kinases (MAPK), which play a crucial role in signal transduction, are activated by phosphorylation in response to a variety of mitogenic signals. In this article, we review the clinical and experimental evidence for brain damage after TBI. In addition, the MAPK pathways, closely involved in signal transduction after TBI, which could therefore be a new and potentially effective therapeutic target in TBI. Further investigations are therefore necessary to better understand cerebral traumatic damage and delineate the best practice strategies needed to improve the patient outcomes after TBI.