T
Teresa de los Santos
Researcher at United States Department of Agriculture
Publications - 62
Citations - 2798
Teresa de los Santos is an academic researcher from United States Department of Agriculture. The author has contributed to research in topics: Virus & Foot-and-mouth disease virus. The author has an hindex of 26, co-authored 52 publications receiving 2477 citations. Previous affiliations of Teresa de los Santos include State University of New York System & Stony Brook University.
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The Mus81/Mms4 endonuclease acts independently of double-Holliday junction resolution to promote a distinct subset of crossovers during meiosis in budding yeast.
Teresa de los Santos,Neil Hunter,Cindy Lee,Brittany Larkin,Josef Loidl,Nancy M. Hollingsworth +5 more
TL;DR: This work provides three lines of evidence that Mus81/Mms4 is not the major meiotic HJ resolvase in S. cerevisiae and reveals the existence of two distinct classes of crossovers in budding yeast.
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The Leader Proteinase of Foot-and-Mouth Disease Virus Inhibits the Induction of Beta Interferon mRNA and Blocks the Host Innate Immune Response
TL;DR: The observation that Lpro controls the transcription of genes involved in innate immunity reveals a novel role of this protein in antagonizing the cellular response to viral infection.
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Meiotic Segregation, Synapsis, and Recombination Checkpoint Functions Require Physical Interaction between the Chromosomal Proteins Red1p and Hop1p
Dana Woltering,Bridget L. Baumgartner,Sandipan Bagchi,Brittany Larkin,Josef Loidl,Teresa de los Santos,Nancy M. Hollingsworth +6 more
TL;DR: Overexpression of HOP1 specifically suppresses red1-K348E, supporting the idea that the only defect in the protein is a reduced affinity for Hop1p, and implicating a role for Red1p-Hop1p hetero-oligomers in these processes.
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Degradation of Nuclear Factor Kappa B during Foot-and-Mouth Disease Virus Infection
TL;DR: The observation that Lpro disrupts the integrity of NF-κB suggests a global mechanism by which FMDV antagonizes the cellular innate immune and inflammatory responses to viral infection.
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Mek1 Kinase Activity Functions Downstream of RED1 in the Regulation of Meiotic Double Strand Break Repair in Budding Yeast
TL;DR: It is proposed that Red1 is phosphorylated by a kinase other than MEK1 and that phosphothreonines on Red1 then interact with the Mek1 FHA domain to recruit the kinase to sites of DSBs where Mek1 is activated to prevent DMC1-independent DSB repair.