Nathan C Manley

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Derivation of injury-responsive dendritic cells for acute brain targeting and therapeutic protein delivery in the stroke-injured rat
    Nathan C Manley
    Department of Biology, Stanford University, Stanford, California, United States of America
    PLoS ONE 8:e61789. 2013
  2. ncbi request reprint Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus
    Nathan C Manley
    Department of Biological Sciences, Stanford University, Stanford, CA, USA
    Brain Res 1182:138-43. 2007
  3. pmc Glucocorticoids increase excitotoxic injury and inflammation in the hippocampus of adult male rats
    Shawn F Sorrells
    Department of Biology, Stanford University, Stanford, Calif, USA
    Neuroendocrinology 100:129-40. 2014
  4. pmc Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain
    Robert H Andres
    Department of Neurosurgery, Stanford Stroke Centre, Stanford Institute for Neuro Innovation and Translational Neurosciences, Stanford University School of Medicine, 1201 Welch Road, Stanford, CA 94305 5487, USA
    Brain 134:1777-89. 2011
  5. pmc Anti-apoptotic therapy with a Tat fusion protein protects against excitotoxic insults in vitro and in vivo
    Kevin L Ju
    Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
    Exp Neurol 210:602-7. 2008
  6. pmc Toxoplasma gondii is dependent on glutamine and alters migratory profile of infected host bone marrow derived immune cells through SNAT2 and CXCR4 pathways
    I Ping Lee
    Department of Biology, Stanford University, Stanford, California, United States of America
    PLoS ONE 9:e109803. 2014
  7. pmc Prokineticin 2 is an endangering mediator of cerebral ischemic injury
    Michelle Y Cheng
    Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 109:5475-80. 2012

Collaborators

Detail Information

Publications7

  1. pmc Derivation of injury-responsive dendritic cells for acute brain targeting and therapeutic protein delivery in the stroke-injured rat
    Nathan C Manley
    Department of Biology, Stanford University, Stanford, California, United States of America
    PLoS ONE 8:e61789. 2013
    ..These results demonstrate a non-invasive method to target ischemic brain injury and may ultimately provide a way to selectively deliver therapeutic compounds to the injured brain...
  2. ncbi request reprint Characterization of monocyte chemoattractant protein-1 expression following a kainate model of status epilepticus
    Nathan C Manley
    Department of Biological Sciences, Stanford University, Stanford, CA, USA
    Brain Res 1182:138-43. 2007
    ....
  3. pmc Glucocorticoids increase excitotoxic injury and inflammation in the hippocampus of adult male rats
    Shawn F Sorrells
    Department of Biology, Stanford University, Stanford, Calif, USA
    Neuroendocrinology 100:129-40. 2014
    ..For some injuries, this GC endangerment of neurons is accompanied by greater immune cell activation in the CNS, a surprising outcome given the potent immunosuppressive properties of GCs...
  4. pmc Human neural stem cells enhance structural plasticity and axonal transport in the ischaemic brain
    Robert H Andres
    Department of Neurosurgery, Stanford Stroke Centre, Stanford Institute for Neuro Innovation and Translational Neurosciences, Stanford University School of Medicine, 1201 Welch Road, Stanford, CA 94305 5487, USA
    Brain 134:1777-89. 2011
    ..Thus, we postulate that human neural progenitor cells aid recovery after stroke through secretion of factors that enhance brain repair and plasticity...
  5. pmc Anti-apoptotic therapy with a Tat fusion protein protects against excitotoxic insults in vitro and in vivo
    Kevin L Ju
    Department of Biological Sciences, Stanford University, Stanford, CA 94305 5020, USA
    Exp Neurol 210:602-7. 2008
    ..This fusion protein decreased neurotoxicity caused by the excitotoxins glutamate and kainic acid in primary hippocampal cultures, and decreased hippocampal damage in vivo in an excitotoxic seizure model...
  6. pmc Toxoplasma gondii is dependent on glutamine and alters migratory profile of infected host bone marrow derived immune cells through SNAT2 and CXCR4 pathways
    I Ping Lee
    Department of Biology, Stanford University, Stanford, California, United States of America
    PLoS ONE 9:e109803. 2014
    ..Thus, our results suggest an important role of glutamine transport via SNAT2 in immune cell migration and a possible interaction between SNAT2 and CXCR4, by which T. gondii manipulates host cell motility. ..
  7. pmc Prokineticin 2 is an endangering mediator of cerebral ischemic injury
    Michelle Y Cheng
    Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 109:5475-80. 2012
    ..These findings indicate that PK2 can be activated by pathological stimuli such as hypoxia-ischemia and excitotoxic glutamate and identify PK2 as a deleterious mediator for cerebral ischemia...