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Chelsea Nora
Researcher at University of California, San Diego
Publications - 8
Citations - 318
Chelsea Nora is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Internal medicine & Heparan sulfate. The author has an hindex of 4, co-authored 6 publications receiving 164 citations. Previous affiliations of Chelsea Nora include University of California, Berkeley.
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Journal ArticleDOI
Statin therapy increases lipoprotein(a) levels.
TL;DR: It is revealed that statins significantly increase plasma Lp(a) levels post-statin therapy and should be studied for effects on residual cardiovascular risk.
Journal ArticleDOI
ApoC-III ASO Promotes Tissue LPL Activity in the Absence of apoE-mediated TRL Clearance
Bastian Ramms,Bastian Ramms,Sohan Patel,Chelsea Nora,Ariane Pessentheiner,Max W. Chang,Courtney R. Green,Gregory J. Golden,Patrick Secrest,Ronald M. Krauss,Christian M. Metallo,Christopher Benner,Veronica J. Alexander,Joseph L. Witztum,Sotirios Tsimikas,Jeffrey D. Esko,Philip L.S.M. Gordts +16 more
TL;DR: The data confirm that ASO-mediated lowering of APOC-III via volanesorsen can reduce plasma TG levels independent of the APOE isoform genotype and establish that apoE is essential to mediate inhibition of TRL clearance by apoC-III.
Journal ArticleDOI
Statins and increases in Lp(a): an inconvenient truth that needs attention.
Journal ArticleDOI
Downstream Products are Potent Inhibitors of the Heparan Sulfate 2-O-Sulfotransferase.
David F. Thieker,Yongmei Xu,Digantkumar Chapla,Chelsea Nora,Hong Qiu,Thomas Felix,Lianchun Wang,Kelley W. Moremen,Jian Liu,Jeffrey D. Esko,Robert J. Woods +10 more
TL;DR: The unexpected finding that oligosaccharides associated with later stages in HS biosynthesis inhibit HS2ST indicates that the enzyme must be separated temporally and/or spatially from downstream products during biosynthesis in vivo, and highlights a challenge for the enzymatic synthesis of lengthy HS chains in vitro.
Posted ContentDOI
The Prolyl-tRNA Synthetase Inhibitor Halofuginone Inhibits SARS-CoV-2 Infection
Daniel R. Sandoval,Thomas Mandel Clausen,Thomas Mandel Clausen,Chelsea Nora,Jason A. Magida,Adam P. Cribbs,Andrea Denardo,Andrea Denardo,Alex E. Clark,Aaron F. Garretson,Joanna K.C. Coker,Anoop Narayanan,Sydney A. Majowicz,Martin Philpott,Catrine Johansson,James E. Dunford,Charlotte B. Spliid,Gregory J. Golden,Gregory J. Golden,N Connor Payne,Mark A Tye,Cameron J. Nowell,Eric R. Griffis,Ann Piermatteo,Kaare V. Grunddal,Thibault Alle,Blake M. Hauser,Jared Feldman,Timothy M. Caradonna,Yuan Pu,Xin Yin,Racheal N. McVicar,Racheal N. McVicar,Elizabeth M. Kwong,Elizabeth M. Kwong,Sotirios Tsimikas,Aaron G. Schmidt,Aaron G. Schmidt,Carlo Ballatore,Karsten Zengler,Sumit K. Chanda,Ryan J. Weiss,Ryan J. Weiss,Micheal Downes,Ronald M. Evans,Ben A. Croker,Sandra L. Leibel,Sandra L. Leibel,Joyce Jose,Ralph Mazitschek,Ralph Mazitschek,Udo Oppermann,Jeffrey D. Esko,Aaron F. Carlin,Philip L.S.M. Gordts +54 more
TL;DR: Halofuginone as discussed by the authors is a compound in clinical trials for anti-fibrotic and anti-inflammatory applications, which is a potent inhibitor of SARS-CoV-2 infection and replication.