Dual leucine zipper kinase is required for excitotoxicity-induced neuronal degeneration
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Jessica L. Larson | K. Scearce-Levie | A. Jubb | R. Weimer | C. Pozniak | Hong Li | Jiansheng Wu | D. Kirkpatrick | Gai Ayalon | Jesse E. Hanson | Joseph W. Lewcock | Daisy J. Bustos | Hai Ngu | Alvin Gogineni | Seung-Hye Lee | Hilda Solanoy | Arundhati Sengupta Ghosh | Qiang Zhou | K. Scearce‐Levie
[1] R. Hanajima,et al. Signaling , 2021, Encyclopedia of Evolutionary Psychological Science.
[2] C. Pozniak,et al. JNK-mediated phosphorylation of DLK suppresses its ubiquitination to promote neuronal apoptosis , 2013, The Journal of cell biology.
[3] Zhiyu Jiang,et al. DLK initiates a transcriptional program that couples apoptotic and regenerative responses to axonal injury , 2013, Proceedings of the National Academy of Sciences.
[4] S. Oliet,et al. Synaptic and Extrasynaptic NMDA Receptors Are Gated by Different Endogenous Coagonists , 2012, Cell.
[5] J. Milbrandt,et al. Dual Leucine Zipper Kinase Is Required for Retrograde Injury Signaling and Axonal Regeneration , 2012, Neuron.
[6] D. J. Cook,et al. Treatment of stroke with a PSD-95 inhibitor in the gyrencephalic primate brain , 2012, Nature.
[7] M. Sheng,et al. The postsynaptic organization of synapses. , 2011, Cold Spring Harbor perspectives in biology.
[8] C. Pozniak,et al. DLK induces developmental neuronal degeneration via selective regulation of proapoptotic JNK activity , 2011, The Journal of cell biology.
[9] T. Blank,et al. Hippocampal c-Jun-N-Terminal Kinases Serve as Negative Regulators of Associative Learning , 2010, The Journal of Neuroscience.
[10] Catherine A. Collins,et al. Protein turnover of the Wallenda/DLK kinase regulates a retrograde response to axonal injury , 2010, The Journal of cell biology.
[11] H. Bading,et al. Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders , 2010, Nature Reviews Neuroscience.
[12] M. Naud,et al. A peptide inhibitor of c-Jun N-terminal kinase for the treatment of endotoxin-induced uveitis. , 2010, Investigative ophthalmology & visual science.
[13] A. Lau,et al. Glutamate receptors, neurotoxicity and neurodegeneration , 2010, Pflügers Archiv - European Journal of Physiology.
[14] M. Bogoyevitch,et al. c-Jun N-terminal kinase (JNK) signaling: recent advances and challenges. , 2010, Biochimica et biophysica acta.
[15] S. Briggs,et al. Sunday Driver Interacts with Two Distinct Classes of Axonal Organelles*♦ , 2009, The Journal of Biological Chemistry.
[16] J. Milbrandt,et al. A dual leucine kinase–dependent axon self-destruction program promotes Wallerian degeneration , 2009, Nature Neuroscience.
[17] V. Bennett,et al. An Ankyrin-Based Mechanism for Functional Organization of Dystrophin and Dystroglycan , 2008, Cell.
[18] S. Sternson,et al. A FLEX Switch Targets Channelrhodopsin-2 to Multiple Cell Types for Imaging and Long-Range Circuit Mapping , 2008, The Journal of Neuroscience.
[19] R. Burke,et al. Antiapoptotic and Trophic Effects of Dominant-Negative Forms of Dual Leucine Zipper Kinase in Dopamine Neurons of the Substantia Nigra In Vivo , 2008, The Journal of Neuroscience.
[20] S. Pfaff,et al. The Ubiquitin Ligase Phr1 Regulates Axon Outgrowth through Modulation of Microtubule Dynamics , 2007, Neuron.
[21] Xiongwei Zhu,et al. c‐Jun phosphorylation in Alzheimer disease , 2007, Journal of neuroscience research.
[22] H. Kiyonari,et al. The c-Jun N-Terminal Kinase Activator Dual Leucine Zipper Kinase Regulates Axon Growth and Neuronal Migration in the Developing Cerebral Cortex , 2006, The Journal of Neuroscience.
[23] O. Steward,et al. Comparison of seizure phenotype and neurodegeneration induced by systemic kainic acid in inbred, outbred, and hybrid mouse strains , 2006, The European journal of neuroscience.
[24] T. Herdegen,et al. JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length , 2006, The Journal of cell biology.
[25] S. Grant,et al. Molecular characterization and comparison of the components and multiprotein complexes in the postsynaptic proteome , 2006, Journal of neurochemistry.
[26] K. Muir. Glutamate-based therapeutic approaches: clinical trials with NMDA antagonists. , 2006, Current opinion in pharmacology.
[27] Hideko Yamamoto,et al. Low concentrations of nitric oxide (NO) induced cell death in PC12 cells through activation of p38 mitogen-activated protein kinase (p38 MAPK) but not via extracellular signal-regulated kinases (ERK1/2) or c-Jun N-terminal protein kinase (JNK) , 2006, Neuroscience Letters.
[28] T. Herdegen,et al. Context-specific inhibition of JNKs: overcoming the dilemma of protection and damage. , 2005, Trends in pharmacological sciences.
[29] J. Zhu,et al. Rap2-JNK Removes Synaptic AMPA Receptors during Depotentiation , 2005, Neuron.
[30] Yanqin Gao,et al. Neuroprotection against Focal Ischemic Brain Injury by Inhibition of c-Jun N-Terminal Kinase and Attenuation of the Mitochondrial Apoptosis-Signaling Pathway , 2005, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[31] W. Gan,et al. Development of Long-Term Dendritic Spine Stability in Diverse Regions of Cerebral Cortex , 2005, Neuron.
[32] M. Ono,et al. Expression of MUK/DLK/ZPK, an activator of the JNK pathway, in the nervous systems of the developing mouse embryo. , 2005, Gene expression patterns : GEP.
[33] F Edward Dudek,et al. Chemoconvulsant Model of Chronic Spontaneous Seizures , 2005, Current protocols in neuroscience.
[34] G. Shepherd,et al. Transient and Persistent Dendritic Spines in the Neocortex In Vivo , 2005, Neuron.
[35] Steven P Gygi,et al. Semiquantitative Proteomic Analysis of Rat Forebrain Postsynaptic Density Fractions by Mass Spectrometry* , 2004, Journal of Biological Chemistry.
[36] Pasko Rakic,et al. JNK-mediated induction of cyclooxygenase 2 is required for neurodegeneration in a mouse model of Parkinson's disease. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[37] Eckart D Gundelfinger,et al. Proteomics Analysis of Rat Brain Postsynaptic Density , 2004, Journal of Biological Chemistry.
[38] P. Rakic,et al. A critical role of neural-specific JNK3 for ischemic apoptosis , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[39] Takashi Yamauchi,et al. Molecular constituents of the postsynaptic density fraction revealed by proteomic analysis using multidimensional liquid chromatography‐tandem mass spectrometry , 2003, Journal of neurochemistry.
[40] A. Vercelli,et al. A peptide inhibitor of c-Jun N-terminal kinase protects against excitotoxicity and cerebral ischemia , 2003, Nature Medicine.
[41] Mark Ellisman,et al. JNK1 is required for maintenance of neuronal microtubules and controls phosphorylation of microtubule-associated proteins. , 2003, Developmental cell.
[42] Yitao Liu,et al. Treatment of Ischemic Brain Damage by Perturbing NMDA Receptor- PSD-95 Protein Interactions , 2002, Science.
[43] T. Herdegen,et al. c-Jun N-Terminal Protein Kinase (JNK) 2/3 Is Specifically Activated by Stress, Mediating c-Jun Activation, in the Presence of Constitutive JNK1 Activity in Cerebellar Neurons , 2002, The Journal of Neuroscience.
[44] Andrew P McMahon,et al. Efficient recombination in diverse tissues by a tamoxifen-inducible form of Cre: a tool for temporally regulated gene activation/inactivation in the mouse. , 2002, Developmental biology.
[45] K. Murai,et al. Contactin Supports Synaptic Plasticity Associated with Hippocampal Long-Term Depression but Not Potentiation , 2002, Current Biology.
[46] N. Nakatsuji,et al. Efficient gene transfer into the embryonic mouse brain using in vivo electroporation. , 2001, Developmental biology.
[47] M. Greenberg,et al. β-Amyloid Induces Neuronal Apoptosis Via a Mechanism that Involves the c-Jun N-Terminal Kinase Pathway and the Induction of Fas Ligand , 2001, The Journal of Neuroscience.
[48] D. Guastella,et al. NMDA But Not Non-NMDA Excitotoxicity is Mediated by Poly(ADP-Ribose) Polymerase , 2000, The Journal of Neuroscience.
[49] M. Kennedy,et al. Identification of Proteins in the Postsynaptic Density Fraction by Mass Spectrometry , 2000, The Journal of Neuroscience.
[50] M Dickens,et al. Interaction of a Mitogen-Activated Protein Kinase Signaling Module with the Neuronal Protein JIP3 , 2000, Molecular and Cellular Biology.
[51] D. Choi,et al. Apoptosis and Necrosis in Cerebrovascular Disease , 1999, Annals of the New York Academy of Sciences.
[52] E. Wagner,et al. Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation , 1999, Nature Genetics.
[53] M. Miller,et al. CEP-1347/KT-7515, an inhibitor of c-jun N-terminal kinase activation, attenuates the 1-methyl-4-phenyl tetrahydropyridine-mediated loss of nigrostriatal dopaminergic neurons In vivo. , 1999, The Journal of pharmacology and experimental therapeutics.
[54] R. Morris,et al. Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein , 1998, Nature.
[55] R. Huganir,et al. SynGAP: a Synaptic RasGAP that Associates with the PSD-95/SAP90 Protein Family , 1998, Neuron.
[56] P. Rakic,et al. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene , 1997, Nature.
[57] William Slikker,et al. Fluoro-Jade: a novel fluorochrome for the sensitive and reliable histochemical localization of neuronal degeneration , 1997, Brain Research.
[58] L. Holzman,et al. Characterization of Dual Leucine Zipper-bearing Kinase, a Mixed Lineage Kinase Present in Synaptic Terminals Whose Phosphorylation State Is Regulated by Membrane Depolarization via Calcineurin* , 1996, The Journal of Biological Chemistry.
[59] T. Dawson,et al. Resistance to neurotoxicity in cortical cultures from neuronal nitric oxide synthase-deficient mice , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[60] Y. Ben-Ari,et al. Apoptosis and Necrosis after Reversible Focal Ischemia: An in Situ DNA Fragmentation Analysis , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[61] S. Lipton,et al. Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function , 1995, Neuron.
[62] S. Lipton,et al. Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[63] A. Contestabile,et al. Protection from kainic acid neuropathological syndrome by NMDA receptor antagonists: Effect of MK-801 and CGP 39551 on neurotransmitter and glial markers , 1992, Neuropharmacology.
[64] Andrew Sherwood. Cervical cytology screening. , 1988, BMJ.
[65] D. Choi,et al. Glutamate neurotoxicity in cortical cell culture is calcium dependent , 1985, Neuroscience Letters.
[66] Y. Ben-Ari,et al. Limbic seizure and brain damage produced by kainic acid: Mechanisms and relevance to human temporal lobe epilepsy , 1985, Neuroscience.
[67] B. Meldrum,et al. Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain. , 1984, Science.
[68] C. Cotman,et al. Postsynaptic density antigens: preparation and characterization of an antiserum against postsynaptic densities , 1981, The Journal of cell biology.
[69] D. J. Cook,et al. Treatment of Stroke , 2014 .
[70] A. Planas,et al. Both apoptosis and necrosis occur following intrastriatal administration of excitotoxins , 2004, Acta Neuropathologica.
[71] A Critical , 2022 .