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Otávio J. B. Brustolini

Researcher at National Institute of Standards and Technology

Publications -  36
Citations -  1341

Otávio J. B. Brustolini is an academic researcher from National Institute of Standards and Technology. The author has contributed to research in topics: Gene & Biology. The author has an hindex of 14, co-authored 31 publications receiving 859 citations. Previous affiliations of Otávio J. B. Brustolini include Universidade Federal de Viçosa.

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Genomic characterization of a novel SARS-CoV-2 lineage from Rio de Janeiro, Brazil

TL;DR: In this article, the authors reported the sequencing of 180 new viral genomes obtained from different municipalities of the state of Rio de Janeiro from April to December 2020, and identified a novel lineage of SARS-CoV-2, originated from B.1.28 lineage, distinguished by five single-nucleotide variants (SNVs): C100U, C28253U, G28628u, G28975U, and C29754U.
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NIK1-mediated translation suppression functions as a plant antiviral immunity mechanism

TL;DR: LIMYB links immune receptor LRR-RLK activation to global translation suppression as an antiviral immunity strategy in plants, which results in protein synthesis inhibition, decreased viral messenger RNA association with polysome fractions and enhanced tolerance to begomovirus.
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The tomato RLK superfamily: phylogeny and functional predictions about the role of the LRRII-RLK subfamily in antiviral defense.

TL;DR: The tomato RLK superfamily is made-up of 647 proteins that form a monophyletic tree with the Arabidopsis RLKs and is divided into 58 subfamilies, which suggests that NIK-mediated antiviral signaling is also likely to operate in tomato, suggesting that tomato NIKs may be good targets for engineering resistance against tomato-infecting begomoviruses.
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The Endoplasmic Reticulum Binding Protein BiP Displays Dual Function in Modulating Cell Death Events

TL;DR: Data indicate that during the hypersensitive PCD, BiP positively regulates the NRP cell death signaling through a yet undefined mechanism that is activated by SA signaling and related to ER functioning, and BiP’s negative regulation of leaf senescence may be linked to its capacity to attenuate the UPR activation and NRPcell death signaling.