R
Regina Shaw
Researcher at Cold Spring Harbor Laboratory
Publications - 3
Citations - 217
Regina Shaw is an academic researcher from Cold Spring Harbor Laboratory. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Neurodegeneration. The author has an hindex of 3, co-authored 3 publications receiving 79 citations.
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Postmortem Cortex Samples Identify Distinct Molecular Subtypes of ALS: Retrotransposon Activation, Oxidative Stress, and Activated Glia.
Oliver H. Tam,Nikolay V. Rozhkov,Regina Shaw,Duyang Kim,Isabel Hubbard,Samantha Fennessey,Nadia Propp,Delphine Fagegaltier,Brent T. Harris,Lyle W. Ostrow,Hemali Phatnani,John Ravits,Josh Dubnau,Molly Hammell +13 more
TL;DR: It is demonstrated that TDP-43 directly binds a subset of retrotransposon transcripts and contributes to their silencing in vitro, and pathological T DP-43 aggregation correlates with retroTransposon de-silencing in vivo.
Posted ContentDOI
Postmortem Cortex Samples Identify Distinct Molecular Subtypes of ALS: Retrotransposon Activation, Oxidative Stress, and Activated Glia
Oliver H. Tam,Nikolay V. Rozhkov,Regina Shaw,Duyang Kim,Isabel Hubbard,Samantha Fennessey,Nadia Propp,Delphine Fagegaltier,Lyle W. Ostrow,Hemali Phatnani,John Ravits,Josh Dubnau,Molly Hammell +12 more
TL;DR: Unbiased analysis of this large survey demonstrated that sporadic ALS patient tissues can be segregated into distinct molecular subsets, demonstrating that at least three distinct molecular signatures contribute to ALS disease.
Journal ArticleDOI
Postmortem Cortex Samples Identify Distinct Molecular Subtypes of ALS: Retrotransposon Activation, Oxidative Stress, and Activated Glia
Oliver H. Tam,Nikolay V. Rozhkov,Regina Shaw,Duyang Kim,Isabel Hubbard,Samantha Fennessey,Nadia Propp,Delphine Fagegaltier,Lyle W. Ostrow,Hemali Phatnani,John Ravits,Josh Dubnau,Molly Hammell +12 more
TL;DR: Using unsupervised machine learning algorithms, the authors stratified the transcriptomes of 148 ALS decedent cortex tissue samples into three distinct and robust molecular subtypes, and demonstrated that at least three distinct molecular signatures contribute to ALS disease.