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Ellen Kanter
Researcher at Columbia University Medical Center
Publications - 18
Citations - 2780
Ellen Kanter is an academic researcher from Columbia University Medical Center. The author has contributed to research in topics: Dopaminergic & Epitope. The author has an hindex of 11, co-authored 14 publications receiving 2115 citations. Previous affiliations of Ellen Kanter include Columbia University.
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Journal ArticleDOI
Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits
Guomei Tang,Kathryn Gudsnuk,Sheng-Han Kuo,Marisa L. Cotrina,Marisa L. Cotrina,Gorazd Rosoklija,Alexander A. Sosunov,Mark S. Sonders,Ellen Kanter,Candace Castagna,Ai Yamamoto,Zhenyu Yue,Ottavio Arancio,Bradley S. Peterson,Frances A. Champagne,Andrew J. Dwork,James E. Goldman,David Sulzer +17 more
TL;DR: This work reports increased dendritic spine density with reduced developmental spine pruning in layer V pyramidal neurons in postmortem ASD temporal lobe and suggests that mTOR-regulated autophagy is required for developmental spinePruning, and activation of neuronal Autophagy corrects synaptic pathology and social behavior deficits in ASD models with hyperactivated mTOR.
Journal ArticleDOI
T cells from patients with Parkinson’s disease recognize α-synuclein peptides
David Sulzer,Roy N. Alcalay,Francesca Garretti,Lucien J. Cote,Ellen Kanter,Julian Agin-Liebes,Christopher Liong,Curtis McMurtrey,William H. Hildebrand,Xiaobo Mao,Valina L. Dawson,Ted M. Dawson,Carla Oseroff,John Pham,John Sidney,Myles B.C. Dillon,Chelsea Carpenter,Daniela Weiskopf,Elizabeth J. Phillips,Elizabeth J. Phillips,Simon Mallal,Simon Mallal,Bjoern Peters,April Frazier,Cecilia S. Lindestam Arlehamn,Alessandro Sette +25 more
TL;DR: It is shown that a defined set of peptides that are derived from α-synuclein, a protein aggregated in Parkinson’s disease, act as antigenic epitopes displayed by these alleles and drive helper and cytotoxic T cell responses in patients with Parkinson's disease.
Journal ArticleDOI
Interplay between Cytosolic Dopamine, Calcium, and α-Synuclein Causes Selective Death of Substantia Nigra Neurons
Eugene V. Mosharov,Kristin E. Larsen,Ellen Kanter,Kester A. Phillips,Krystal Wilson,Yvonne Schmitz,David E. Krantz,Kazuto Kobayashi,Robert H. Edwards,David Sulzer +9 more
TL;DR: Using intracellular patch electrochemistry to directly measure cytosolic dopamine in cultured midbrain neurons, it is confirmed that elevated DA(cyt) and its metabolites are neurotoxic and that genetic and pharmacological interventions that decrease DA(Cyt) provide neuroprotection.
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MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration
Carolina Cebrián,Fabio A. Zucca,Pierluigi Mauri,Julius A. Steinbeck,Lorenz Studer,Clemens R. Scherzer,Ellen Kanter,Sadna Budhu,Jonathan Mandelbaum,Jean Paul Vonsattel,Luigi Zecca,John D. Loike,David Sulzer +12 more
TL;DR: Evidence is provided from immunolabel, RNA expression, and mass spectrometry analysis of postmortem samples that human catecholaminergic substantia nigra and locus coeruleus neurons express MHC-I, and that this molecule is inducible in human stem cell derived dopamine (DA) neurons.
Journal ArticleDOI
Mitochondrial dysfunction and mitophagy defect triggered by heterozygous GBA mutations
Hongyu Li,Ahrom Ham,Thong C. Ma,Sheng-Han Kuo,Ellen Kanter,Dong-Hoon Kim,Han Seok Ko,Yi Quan,Sergio Pablo Sardi,Aiqun Li,Ottavio Arancio,Un Jung Kang,David Sulzer,Guomei Tang +13 more
TL;DR: It is shown that in GbaL444P/WT knockin mice, the L444P heterozygous Gba mutation triggers mitochondrial dysfunction by inhibiting autophagy and mitochondrial priming, two steps critical for the selective removal of dysfunctional mitochondria by Autophagy, a process known as mitophagy.