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Sean M. Riordan

Researcher at Children's Mercy Hospital

Publications -  24
Citations -  902

Sean M. Riordan is an academic researcher from Children's Mercy Hospital. The author has contributed to research in topics: Kernicterus & Medicine. The author has an hindex of 11, co-authored 21 publications receiving 726 citations. Previous affiliations of Sean M. Riordan include University of Kansas & University of Missouri–Kansas City.

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Journal ArticleDOI

Axonal BACE1 dynamics and targeting in hippocampal neurons: a role for Rab11 GTPase

TL;DR: The results reveal novel information on dynamic BACE1 transport in neurons, and demonstrate that Rab11-GTPase function is critical for axonal sorting of Bace1.
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Intraneuronal Aβ detection in 5xFAD mice by a new Aβ-specific antibody

TL;DR: Both intraneuronal Aβ accumulation and extracellular A β deposition was demonstrated in 5xFAD mice and 3xTg mice with MOAB-2, an antibody that will help differentiate intracellular Aβ from APP, however, further investigation is required to determine whether a molecular mechanism links the presence of intraneuonal A β with neurotoxicity.
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β-Site Amyloid Precursor Protein (APP)-cleaving Enzyme 1 (BACE1)-deficient Mice Exhibit a Close Homolog of L1 (CHL1) Loss-of-function Phenotype Involving Axon Guidance Defects *♦

TL;DR: The results imply the possibility that axon mis-targeting may occur in adult neurogenic and/or regenerating neurons as a result of chronic Bace1 inhibition and add a note of caution to BACE1 inhibitor development.
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The Neurological Sequelae of Neonatal Hyperbilirubinemia: Definitions, Diagnosis and Treatment of the Kernicterus Spectrum Disorders (KSDs).

TL;DR: Adopting a systematic nomenclature for the spectrum of clinical consequences of hyperbilirubinemia will help unify the field and promote more effective research in both prevention and treatment of KSDs.
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Epac2 Mediates cAMP-Dependent Potentiation of Neurotransmission in the Hippocampus.

TL;DR: Examination of synaptic transmission during long sustained trains of activity suggested that the readily releasable pool of vesicles is reduced in Epac2−/− mice, and data suggest that cAMP elevation uses an Epac 2-dependent pathway to promote transmitter release, and thatEpac2 is required to maintain the readily RELEASable pool at MF synapses in the hippocampus.