ArticleLife science alliance2026
Enzymes of physiological amyloidogenesis control pathological amyloid toxicity.
Michael Bokros, Alex Grunfeld, Nathan C Balukoff, Jessica Bouviere, Eléonore Beurel, Stephen Lee
Abstract read
In one paragraphArticle in Life science alliance, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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2 · The registryThe trial behind it
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
6 authors.
Michael BokrosDepartment of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Alex GrunfeldDepartment of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Nathan C BalukoffDepartment of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Jessica BouviereDepartment of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Eléonore BeurelDepartment of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL, USA.
Stephen LeeDepartment of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL, USA stephenlee@med.miami.edu.ORCID 0000-0001-7517-8186 Funding
Th17 cells as a new therapeutic target for depressionR01MH104656 · NIMH · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BEUREL, ELEONORE · 2015 to 2024
$3.8MThe Nucleolar Detention Center: a Hub of Long Noncoding RNAs that Imprison Proteins During StressR01GM115342 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LEE, STEPHEN · 2015 to 2022
$2.6MAmyloid-bodies and the Evolution of MalignanciesR01CA275828 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Stephen Lee · 2023 to 2026
$1.6MThe Nucleolar Detention Center: A Hub of Long Noncoding RNA that Imprison Proteins during StressR35GM149221 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Stephen Lee · 2023 to 2026
$1.5MUncovering an Enzymatic Program that Drives Physiological and Pathological Amyloid Formation.K99AG080474 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BOKROS, MICHAEL · 2023 to 2024
$187kNCI NIH HHS R01 CA275828NIA NIH HHS K99 AG080474NIGMS NIH HHS R01 GM115342NIGMS NIH HHS R35 GM149221NIMH NIH HHS R01 MH104656
6 · The paper itselfAbstract
Physiological amyloidogenesis drives the formation of functional amyloids involved in various biochemical pathways. We recently showed that the RNA tailing and decay machinery controls the maturation of intracellular amyloid-like aggregates. This raises the question of whether enzymes that participate in the maturation of physiological amyloids are involved in pathological amyloidogenesis implicated in human proteopathies. Using
Indexed as
AmyloidAmyloid beta-Peptidesalpha-SynucleinAlzheimer DiseaseAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDisease Models, AnimalHumansMiceRNA-Binding Proteinsalpha-SynucleinAmyloidAmyloid beta-PeptidesCaenorhabditis elegans ProteinsRNA-Binding Proteins
Identifiers
PMID41850724
PMCPMC13000121
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