Next Article in Journal
(Healthy) Ageing: Focus on Iodothyronines
Next Article in Special Issue
Exposure to Environmental Toxicants and Pathogenesis of Amyotrophic Lateral Sclerosis: State of the Art and Research Perspectives
Previous Article in Journal
Molecular and Functional Imaging for Detection of Lymph Node Metastases in Prostate Cancer
Article Menu

Export Article

Open AccessReview
Int. J. Mol. Sci. 2013, 14(7), 13858-13872;

Death Associated Protein Kinases: Molecular Structure and Brain Injury

Institute of Neuroscience and Physiology, Sahlgrenska Academy, Gothenburg University, Gothenburg 40530, Sweden
School of Biotechnology, National Institute of Technology Calicut, Calicut 673601, India
Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg University, Gothenburg 40530, Sweden
Centre for the Developing Brain, Division of Imaging Sciences & Biomedical Engineering, The Rayne Institute, King's College London St Thomas' Hospital, London SE1 7EH, UK
Author to whom correspondence should be addressed.
Received: 24 May 2013 / Revised: 14 June 2013 / Accepted: 27 June 2013 / Published: 4 July 2013
(This article belongs to the Special Issue Molecular Research in Neurotoxicology)
Full-Text   |   PDF [2204 KB, uploaded 19 June 2014]   |  


Perinatal brain damage underlies an important share of motor and neurodevelopmental disabilities, such as cerebral palsy, cognitive impairment, visual dysfunction and epilepsy. Clinical, epidemiological, and experimental studies have revealed that factors such as inflammation, excitotoxicity and oxidative stress contribute considerably to both white and grey matter injury in the immature brain. A member of the death associated protein kinase (DAPk) family, DAPk1, has been implicated in cerebral ischemic damage, whereby DAPk1 potentiates NMDA receptor-mediated excitotoxicity through interaction with the NR2BR subunit. DAPk1 also mediate a range of activities from autophagy, membrane blebbing and DNA fragmentation ultimately leading to cell death. DAPk mRNA levels are particularly highly expressed in the developing brain and thus, we hypothesize that DAPk1 may play a role in perinatal brain injury. In addition to reviewing current knowledge, we present new aspects of the molecular structure of DAPk domains, and relate these findings to interacting partners of DAPk1, DAPk-regulation in NMDA-induced cerebral injury and novel approaches to blocking the injurious effects of DAPk1. View Full-Text
Keywords: DAPk1; neuroprotection; neonatal hypoxia-ischemia; NMDA receptor DAPk1; neuroprotection; neonatal hypoxia-ischemia; NMDA receptor

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Share & Cite This Article

MDPI and ACS Style

Nair, S.; Hagberg, H.; Krishnamurthy, R.; Thornton, C.; Mallard, C. Death Associated Protein Kinases: Molecular Structure and Brain Injury. Int. J. Mol. Sci. 2013, 14, 13858-13872.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top