Research Topics
Genomes and Genes
| S A LiptonSummaryAffiliation: Harvard University Country: USA Publications
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Detail Information
Publications
Neuropathogenesis of acquired immunodeficiency syndrome dementiaS A Lipton
Laboratory of Cellular and Molecular Neuroscience, Harvard Medical School and Children s Hospital, Boston MA, USA
Curr Opin Neurol 10:247-53. 1997..Some of these potential new treatments have now entered clinical trials...
Neurotoxicity associated with dual actions of homocysteine at the N-methyl-D-aspartate receptorS A Lipton
Laboratory of Cellular and Molecular Neuroscience, Children s Hospital, and Program in Neuroscience, Harvard Medical School, 300 Longwood Avenue, Enders Building, Suite 361, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 94:5923-8. 1997..Accordingly, homocysteine neurotoxicity through overstimulation of N-methyl-D-aspartate receptors may contribute to the pathogenesis of both homocystinuria and modest hyperhomocysteinemia...- Similarity of neuronal cell injury and death in AIDS dementia and focal cerebral ischemia: potential treatment with NMDA open-channel blockers and nitric oxide-related speciesS A Lipton
Laboratory of Cellular and Molecular Neuroscience, Children s Hospital, Boston, Massachusetts 02115, USA
Brain Pathol 6:507-17. 1996..With the very recent development of clinically-tolerated NMDA antagonists, as discussed here, there is hope for future pharmacological intervention... - Neuroprotective versus neurodestructive effects of NO-related speciesS A Lipton
CNS Research Institute, Brigham and Women s Hospital, Boston, MA 02115, USA
Biofactors 8:33-40. 1998.... - ICAM-1 dependent pathway is not involved in the development of neuronal apoptosis after transient focal cerebral ischemiaS G Soriano
Department of Anesthesia, Children s Hospital, Boston 02115, USA
Brain Res 780:337-41. 1998..ICAM-1 deficiency minimizes necrosis but not apoptosis after temporary MCAO in mice, thereby leaving the potential for delayed neuronal cell death despite ICAM-1 inactivation... - hMEF2C gene encodes skeletal muscle- and brain-specific transcription factorsJ C McDermott
Howard Hughes Medical Institute, Children s Hospital, Boston, Massachusetts
Mol Cell Biol 13:2564-77. 1993.... - Assignment of human myocyte-specific enhancer binding factor 2C (hMEF2C) to human chromosome 5q14 and evidence that MEF2C is evolutionarily conservedD Krainc
Department of Neurology, Children's Hospital, Boston, Massachusetts 02115, USA
Genomics 29:809-11. 1995 - Evidence for coassembly of mutant GABAC rho1 with GABAA gamma2S, glycine alpha1 and glycine alpha2 receptor subunits in vitroZ H Pan
CNS Research Institute, Brigham and Women s Hospital and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
Eur J Neurosci 12:3137-45. 2000.... - Cloning and characterization of mouse GABA(C) receptor subunitsA Greka
Cerebrovascular and NeuroScience Research Institute, Brigham and Woman s Hospital, Boston, MA 02115, USA
Neuroreport 9:229-32. 1998..Mouse rho1 and rho2 also co-assemble to form heteromeric receptors. These findings form the basis for further study on GABA(C) receptors using the mouse model... - Synergistic activation of the N-methyl-D-aspartate receptor subunit 1 promoter by myocyte enhancer factor 2C and Sp1D Krainc
CNS Research Institute, Brigham and Women s Hospital, and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 273:26218-24. 1998.... - Mice deficient in Mac-1 (CD11b/CD18) are less susceptible to cerebral ischemia/reperfusion injuryS G Soriano
Department of Anesthesia, Children s Hospital, Boston, MA 02115, USA
Stroke 30:134-9. 1999..To determine the role of Mac-1 during ischemia and reperfusion in the brain, we analyzed the effect of transient focal cerebral ischemia in mice genetically engineered with a specific deficiency in Mac-1... - Redox modulation of the NMDA receptor by NO-related speciesS A Lipton
CNS Research Institute, Brigham and Women s Hospital, and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
Prog Brain Res 118:73-82. 1998..Thus, this chemical reaction is gaining acceptance as a newly-recognized molecular switch to control protein function via reactive thiol groups such as those encountered on the NMDA receptor... - Chemokines and activated macrophages in HIV gp120-induced neuronal apoptosisM Kaul
CNS Research Institute, Brigham and Women s Hospital, and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 96:8212-6. 1999..Moreover, gp120SF2-induced neuronal apoptosis depends predominantly on an indirect pathway via activation of chemokine receptors on macrophages/microglia, whereas SDF-1 may act directly on neurons or astrocytes... - Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3AS Das
Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature 393:377-81. 1998..These data suggest that NR3A is involved in the development of synaptic elements by modulating NMDAR activity... - Neuronal injury associated with HIV-1: approaches to treatmentS A Lipton
Cerebrovascular and NeuroScience Research Institute, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
Annu Rev Pharmacol Toxicol 38:159-77. 1998..With the very recent development of clinically tolerated NMDA antagonists, there is hope for future pharmacological intervention... - Intercellular adhesion molecule-1-deficient mice are less susceptible to cerebral ischemia-reperfusion injuryS G Soriano
Department of Anesthesia Children s Hospital, Boston, MA 02115, USA
Ann Neurol 39:618-24. 1996..These data support the premise that neutrophil adhesion in ischemic areas may be deleterious and that ICAM-1 deficiency reduces neurological damage after transient focal cerebral ischemia... - Calcium, free radicals and excitotoxins in neuronal apoptosisS A Lipton
CNS Research Institute, Brigham and Women s Hospital, Boston, Massachusetts, USA
Cell Calcium 23:165-71. 1998..In collaboration, our two research laboratories have been defining excitotoxic signals that lead to apoptosis versus necrosis via, among other pathways, Ca2+ signaling mechanisms; this is the subject of this brief review... - The coat protein gp120 of HIV-1 inhibits astrocyte uptake of excitatory amino acids via macrophage arachidonic acidE B Dreyer
Department of Ophthalmology, Harvard Medical School, Boston, MA 02115, USA
Eur J Neurosci 7:2502-7. 1995..Our findings suggest that the observed effects on glia and neurons of gp120 may be secondary, at least in part, to its initial activation of macrophages... - Cloning of a gamma-aminobutyric acid type C receptor subunit in rat retina with a methionine residue critical for picrotoxinin channel blockD Zhang
Laboratory of Cellular and Molecular Neuroscience, Children s Hospital, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 92:11756-60. 1995..This study reveals not only the molecular mechanism underlying PTX blockade of GABA receptors but also the heteromeric nature of native receptors in the rat retina that underlie the PTX-resistant GABAC response... - MEF2C, a MADS/MEF2-family transcription factor expressed in a laminar distribution in cerebral cortexD Leifer
Department of Neurology, Children s Hospital, Boston, MA
Proc Natl Acad Sci U S A 90:1546-50. 1993..The unusual pattern of expression in brain suggests that this transcription factor may be important in the development of cortical architecture... - Neuroprotection by the NMDA receptor-associated open-channel blocker memantine in a photothrombotic model of cerebral focal ischemia in neonatal ratP E Stieg
CNS Research Institute, Neurosurgical Service, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Eur J Pharmacol 375:115-20. 1999..0001). At this dosage, memantine manifests few, if any, neurobehavioral side effects. Thus memantine appears to be both safe and effective in neonatal as well as adult animal models of stroke... - Neuronal protection and destruction by NOS A Lipton
The CNS Research Institute, Brigham and Women s Hospital, and Program in Neuroscience, Harvard Medical School, Boston, MA 02115 USA
Cell Death Differ 6:943-51. 1999..NO- -unlike NO* but reminiscent of NO+ transfer - reacts with critical thiol groups of the NMDA receptor to curtail excessive Ca2+ influx and thus provide neuroprotection from excitotoxic insults... - An astrocytic binding site for neuronal Thy-1 and its effect on neurite outgrowthE B Dreyer
Laboratory of Cellular and Molecular Neuroscience, Children s Hospital, Boston, MA, USA
Proc Natl Acad Sci U S A 92:11195-9. 1995..The Thy-1-binding protein may participate in axonal or dendritic development in the nervous system... - Potential and current use of N-methyl-D-aspartate (NMDA) receptor antagonists in diseases of agingD A Le
Stroke and Neurovascular Regulation Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
Drugs Aging 18:717-24. 2001..In this review, we present the evidence that clinically safer NMDA antagonists such as memantine and nitroglycerin, and the combination drug nitro-memantine, are promising as drugs in treating neurodegenerative diseases...