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Patricia Spilman

Researcher at University of California, Los Angeles

Publications -  56
Citations -  2109

Patricia Spilman is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Antigen & Medicine. The author has an hindex of 15, co-authored 48 publications receiving 1666 citations. Previous affiliations of Patricia Spilman include University of California & Buck Institute for Research on Aging.

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Molecular dynamic simulation reveals E484K mutation enhances spike RBD-ACE2 affinity and the combination of E484K, K417N and N501Y mutations (501Y.V2 variant) induces conformational change greater than N501Y mutant alone, potentially resulting in an escape mutant

TL;DR: In this article, a simulation of the spike receptor binding domain (S RBD) and its binding to human angiotensin-converting enzyme 2 (hACE2) was used to predict alterations in molecular interactions resulting from the presence of the E484K, K417N, and N501Y variants found in the South African 501Y.1.V2 strain.
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In vivo oxidative stress in brain of Alzheimer disease transgenic mice: Requirement for methionine 35 in amyloid β-peptide of APP

TL;DR: This is the first in vivo study to demonstrate the requirement for Abeta residue Met35 for oxidative stress in the brain of a mammalian model of Alzheimer disease, and it is shown that oxidative stress is neither required nor sufficient for memory abnormalities.
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PrPc Glycoform Heterogeneity as a Function of Brain Region: Implications for Selective Targeting of Neurons by Prion Strains

TL;DR: The hypothesis that thePrP(Sc) accumulation and the vacuolation pattern phenotypes in the brain are governed by neuron-specific differences in PrP(C) glycoforms is supported.
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Direct Transcriptional Effects of Apolipoprotein E

TL;DR: It is shown for the first time that apolipoprotein E4 binds DNA with high affinity and that its binding sites include 1700 promoter regions that include genes associated with neurotrophins, programmed cell death, synaptic function, sirtuins and aging, and insulin resistance, all processes that have been implicated in Alzheimer's disease pathogenesis.