Genomes and Genes
Affiliation: Imperial College
- Molecular mechanisms of neonatal brain injuryClaire Thornton
Centre for the Developing Brain, Institute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
Neurol Res Int 2012:506320. 2012..We review some of the critical molecular events related to mitochondrial dysfunction and apoptosis during the secondary phase and report some recent evidence that intervention may be feasible also days-weeks after the insult...
- Muscarinic receptor activation of AMP-activated protein kinase inhibits orexigenic neuropeptide mRNA expressionClaire Thornton
Medical Research Council MRC Cellular Stress Group, MRC Clinical Sciences Centre, Du Cane Road, London W12 0NN, United Kingdom
J Biol Chem 283:17116-22. 2008..These data support a hypothesis that modulating basal AMPK activity in the hypothalamus is essential for maintaining tight regulation of pathways contributing to food intake...
- AMP-activated protein kinase (AMPK) is a tau kinase, activated in response to amyloid β-peptide exposureClaire Thornton
Cellular Stress Group, MRC Clinical Sciences Centre, London, UK
Biochem J 434:503-12. 2011..These findings identify a pathway in which Aβ-(1-42) activates CaMKKβ and AMPK via the NMDA receptor, suggesting the possibility that AMPK plays a role in the pathophysiological phosphorylation of tau...
- A dual role for AMP-activated protein kinase (AMPK) during neonatal hypoxic-ischaemic brain injury in miceCatherine I Rousset
Division of Imaging Sciences and Biomedical Engineering, Centre for the Developing Brain, King s College London, King s Health Partners, St Thomas Hospital, London, UK
J Neurochem 133:242-52. 2015..Our data have clinical relevance as prior sensitization (e.g. exposure to bacterial infection reducing AMPK activity) increases injury. AMPK, AMP-activated protein kinase; HI, hypoxia-ischaemia; OGD, oxygen-glucose deprivation. ..
- Mitochondria: hub of injury responses in the developing brainHenrik Hagberg
Centre for the Developing Brain, Perinatal Imaging and Health, King s College London, St Thomas Hospital, London, UK Perinatal Center, Departments of Clinical Sciences and Physiology and Neurosciences, Sahlgrenska Academy, Sahlgrenska University Hospital, Gothenburg, Sweden Electronic address
Lancet Neurol 13:217-32. 2014..Understanding of these new aspects of mitochondrial function will provide insights into brain development and neurological disease, and enable discovery and development of new strategies for treatment. ..
- Investigating the regulation of brain-specific kinases 1 and 2 by phosphorylationNicola J Bright
Medical Research Council Cellular Stress Group, MRC Clinical Sciences Centre, Du Cane Road, London, United Kingdom
J Biol Chem 283:14946-54. 2008..Furthermore, stimuli that activate AMPK had no effect on BRSK1/2. Finally, we provide evidence suggesting that protein phosphatase 2C is a likely candidate for catalyzing the dephosphorylation and inactivation of BRSK1/2...
- Effect of Trp53 gene deficiency on brain injury after neonatal hypoxia-ischemiaAna A Baburamani
Perinatal Brain Injury Group, Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King s College London, King s Health Partners, St Thomas Hospital, London, United Kingdom
Oncotarget . 2017..These data suggest that p53 has a limited contribution to the development of injury in the immature/juvenile brain following HI. Further studies are required to determine the effect of p53 on downstream targets...
- The Anti-Inflammatory Effects of the Small Molecule Pifithrin-µ on BV2 MicrogliaBobbi Fleiss
Department of Perinatal Imaging and Health, Division of Imaging Sciences and Biomedical Engineering, King s College London, King s Health Partners, St Thomas Hospital, London, UK
Dev Neurosci 37:363-75. 2015..This study demonstrates that the neuroprotective effects of PFT-µ in HI-induced NE may include an anti-inflammatory effect on microglia and adds to the evidence that this drug might be of clinical interest for the treatment of NE...
- Mitochondrial Optic Atrophy (OPA) 1 Processing Is Altered in Response to Neonatal Hypoxic-Ischemic Brain InjuryAna A Baburamani
Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King s College London, St Thomas Hospital, SE1 7EH London, UK
Int J Mol Sci 16:22509-26. 2015..Our data strongly suggest that alterations in mitochondria-shaping proteins are an early event in the pathogenesis of neonatal HI injury. ..
- Mitochondria and perinatal brain injuryCatherine I Rousset
Centre for the Developing Brain, Institute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Imperial College, Hammersmith Campus, London, UK
J Matern Fetal Neonatal Med 25:35-8. 2012..In this brief review, we update the critical role of mitochondria in brain development and the decision of cell fate after hypoxia-ischemia in the immature CNS...
- Role of mitochondria in apoptotic and necroptotic cell death in the developing brainClaire Thornton
Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King s College London, King s Health Partners, St Thomas Hospital, London SE1 7EH, United Kingdom
Clin Chim Acta 451:35-8. 2015..Death receptors trigger apoptotic death via caspase-8 and necroptotic cell death through formation of the necrosome (composed of RIP1, RIP3 and MLKL), both of which converge at the mitochondria. ..
- AMP-activated protein kinase: new regulation, new roles?David Carling
Cellular Stress Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, DuCane Road, London, W12 0NN, UK
Biochem J 445:11-27. 2012....
- Mind bomb-2 is an E3 ligase that ubiquitinates the N-methyl-D-aspartate receptor NR2B subunit in a phosphorylation-dependent mannerRachel Jurd
Gallo Research Center, Department of Neurology, University of California San Francisco, Emeryville, CA 94608, USA
J Biol Chem 283:301-10. 2008..These results identify a specific E3 ubiquitin ligase as a novel interactant with the NR2B subunit and suggest a possible mechanism for the regulation of NMDAR function involving both phosphorylation and ubiquitination...
- H-Ras modulates N-methyl-D-aspartate receptor function via inhibition of Src tyrosine kinase activityClaire Thornton
Ernest Gallo Clinic and Research Center, University of California San Francisco, San Francisco, California 94110 3518, USA
J Biol Chem 278:23823-9. 2003..This mechanism is specific for Src and NR2A and has implications for studies in which regulation of NMDA receptor-mediated LTP is important, such as synaptic plasticity, learning, and memory and addiction...
- NMDA receptor function is regulated by the inhibitory scaffolding protein, RACK1Rami Yaka
Ernest Gallo Clinic and Research Center, University of California, San Francisco, CA 94110 3518, USA
Proc Natl Acad Sci U S A 99:5710-5. 2002..Therefore, RACK1 is a regulator of NMDA receptor function and may play a role in synaptic plasticity, addiction, learning, and memory...