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Luis Martinez-Sobrido

Researcher at Texas Biomedical Research Institute

Publications -  287
Citations -  14829

Luis Martinez-Sobrido is an academic researcher from Texas Biomedical Research Institute. The author has contributed to research in topics: Virus & Influenza A virus. The author has an hindex of 52, co-authored 226 publications receiving 11478 citations. Previous affiliations of Luis Martinez-Sobrido include University of Rochester Medical Center & Icahn School of Medicine at Mount Sinai.

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Distinct RIG-I and MDA5 Signaling by RNA Viruses in Innate Immunity

TL;DR: Differential and redundant roles for RIG-I and MDA5 in pathogen recognition and innate immune signaling that may reflect unique and shared biologic properties of RNA viruses whose differential triggering and control of gene expression may impact pathogenesis and infection are demonstrated.
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Severe Acute Respiratory Syndrome Coronavirus Open Reading Frame (ORF) 3b, ORF 6, and Nucleocapsid Proteins Function as Interferon Antagonists

TL;DR: It has been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response.
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Discovery of SARS-CoV-2 antiviral drugs through large-scale compound repurposing.

TL;DR: A screen of the ReFRAME library of approximately 12,000 known drugs for antiviral activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) identified several candidate compounds with suitable activities and pharmacological profiles, which could potentially expedite the deployment of therapies for coronav virus disease 2019 (COVID-19).
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Inhibition of Retinoic Acid-Inducible Gene I-Mediated Induction of Beta Interferon by the NS1 Protein of Influenza A Virus

TL;DR: The results indicate that, in addition to sequestering dsRNA, the NS1 of influenza A virus binds to RIG-I and inhibits downstream activation of IRF-3, preventing the transcriptional induction of IFN-β.
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Inhibition of Alpha/Beta Interferon Signaling by the NS4B Protein of Flaviviruses

TL;DR: Deletion analysis shows that that the first 125 amino acids of dengue virus NS4B are sufficient for inhibition of alpha/beta IFN (IFN-α/β) signaling, indicating that proper viral polyprotein processing is required for anti-interferon function.