N
Nikolaos K. Robakis
Researcher at Icahn School of Medicine at Mount Sinai
Publications - 124
Citations - 9280
Nikolaos K. Robakis is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Amyloid precursor protein & Presenilin. The author has an hindex of 53, co-authored 120 publications receiving 8953 citations. Previous affiliations of Nikolaos K. Robakis include Mount Sinai Hospital & New York State Office for People With Developmental Disabilities.
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A presenilin‐1/γ‐secretase cleavage releases the E‐cadherin intracellular domain and regulates disassembly of adherens junctions
Philippe Marambaud,Junichi Shioi,Geo Serban,Anastasios Georgakopoulos,Shula Sarner,Vanja Nagy,Lia Baki,Paul H. Wen,Spiros Efthimiopoulos,Zhiping Shao,Thomas Wisniewski,Nikolaos K. Robakis +11 more
TL;DR: It is shown that presenilin‐1 (PS1), a protein involved in Alzheimer's disease, controls a γ‐secretase‐like cleavage of E‐cadherin that stimulates disassembly of the E‐ cadher in– catenin complex and increases the cytosolic pool of β‐catenin, a key regulator of the Wnt signaling pathway.
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Molecular cloning and characterization of a cDNA encoding the cerebrovascular and the neuritic plaque amyloid peptides.
TL;DR: Localization of the corresponding genomic sequences on human chromosome 21 suggests a genetic relationship between Alzheimer disease and Down syndrome, and it may explain the early appearance of large numbers of neuritic plaques in adult Down syndrome patients.
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A CBP Binding Transcriptional Repressor Produced by the PS1/ϵ-Cleavage of N-Cadherin Is Inhibited by PS1 FAD Mutations
Philippe Marambaud,Paul H. Wen,Anindita Dutt,Junichi Shioi,Akihiko Takashima,Robert Siman,Nikolaos K. Robakis +6 more
TL;DR: It is shown that a PS1-dependent gamma-secretase protease activity promotes an epsilon-like cleavage of N-cadherin to produce its intracellular domain peptide, N-Cad/CTF2, which functions as a potent repressor of CBP/CREB-mediated transcription.
Journal Article
Immunohistochemical evidence of oxidative [corrected] stress in Alzheimer's disease.
TL;DR: The hypothesis that oxidative stress may be involved in the pathogenesis of Alzheimer's disease is supported.
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PS1 activates PI3K thus inhibiting GSK‐3 activity and tau overphosphorylation: effects of FAD mutations
Lia Baki,Junichi Shioi,Paul H. Wen,Zhiping Shao,A. L. Schwarzman,Miguel Gama-Sosa,Rachael L. Neve,Nikolaos K. Robakis +7 more
TL;DR: It is shown that PS1, a protein involved in familial Alzheimer's disease (FAD), promotes cell survival by activating the PI3K/Akt cell survival signaling, and this function of PS1 is unaffected by γ‐secretase inhibitors.