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Joseph Hiatt

Researcher at University of California, San Francisco

Publications -  45
Citations -  8119

Joseph Hiatt is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Genome editing & T cell. The author has an hindex of 20, co-authored 38 publications receiving 5422 citations. Previous affiliations of Joseph Hiatt include National Institutes of Health & University of California, Berkeley.

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A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.

David E. Gordon, +128 more
- 30 Apr 2020 - 
TL;DR: A human–SARS-CoV-2 protein interaction map highlights cellular processes that are hijacked by the virus and that can be targeted by existing drugs, including inhibitors of mRNA translation and predicted regulators of the sigma receptors.
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Detection of ultra-rare mutations by next-generation sequencing

TL;DR: It is determined that Duplex Sequencing has a theoretical background error rate of less than one artifactual mutation per billion nucleotides sequenced and that detection of mutations present in only one of the two strands of duplex DNA can be used to identify sites of DNA damage.
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The Global Phosphorylation Landscape of SARS-CoV-2 Infection.

Mehdi Bouhaddou, +77 more
- 06 Aug 2020 - 
TL;DR: A quantitative mass spectrometry-based phosphoproteomics survey of SARS-CoV-2 infection in Vero E6 cells reveals dramatic rewiring of phosphorylation on host and viral proteins, revealing potential COVID-19 therapies.
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Reprogramming human T cell function and specificity with non-viral genome targeting

TL;DR: A non-viral strategy to introduce large DNA sequences into T cells enables the correction of a pathogenic mutation that causes autoimmunity, and the replacement of an endogenous T-cell receptor with an engineered receptor that can recognize cancer antigens.
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Comparative host-coronavirus protein interaction networks reveal pan-viral disease mechanisms.

David E. Gordon, +203 more
- 04 Dec 2020 - 
TL;DR: The authors identified shared biology and host-directed drug targets to prioritize therapeutics with potential for rapid deployment against current and future coronavirus outbreaks, and found that individuals with genotypes corresponding to higher soluble IL17RA levels in plasma are at decreased risk of COVID-19 hospitalization.