Publications by authors named "Matthew W Kenaston"

Article Synopsis
  • Autophagy plays a crucial role in various diseases, making it a promising target for therapies, yet its mechanisms are still not fully understood due to limited systematic measurements.
  • Recent studies by Loos et al. (2014) and Beesabathuni et al. (2022) have introduced methods for quantitatively measuring autophagy, which could help clarify its role in diseases.
  • This commentary discusses unresolved questions in autophagy research and highlights the importance of rate measurements for developing cancer treatments and understanding virus interactions, suggesting a need for advanced screening methods to unravel autophagy's complexities.
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In the ongoing arms race between virus and host, fine-tuned gene expression plays a critical role in antiviral signaling. However, viruses have evolved to disrupt this process and promote their own replication by targeting host restriction factors. Polymerase-associated factor 1 complex (PAF1C) is a key player in this relationship, recruiting other host factors to regulate transcription and modulate innate immune gene expression.

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Background: Sitting at the interface of gene expression and host-pathogen interaction, polymerase associated factor 1 complex (PAF1C) is a rising player in the innate immune response. The complex localizes to the nucleus and associates with chromatin to modulate RNA polymerase II (RNAPII) elongation of gene transcripts. Performing this function at both proximal and distal regulatory elements, PAF1C interacts with many host factors across such sites, along with several microbial proteins during infection.

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SARS-CoV-2 Spike is a key protein that mediates viral entry into cells and elicits antibody responses. Its importance in infection, diagnostics, and vaccinations has created a large demand for purified Spike for clinical and research applications. Spike is difficult to express, prompting modifications to the protein and expression platforms to improve yields.

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Article Synopsis
  • Viruses rely on host cells' machinery to replicate, often interfering with host protein functions, which can lead to diseases that benefit the virus or occur by chance.
  • Understanding how viruses interact with host proteins helps reveal the molecular processes behind virus replication and disease caused by these infections.
  • The review discusses systems biology methods for identifying virus-host interactions and innovations that help researchers transition from generating hypotheses to understanding mechanisms more quickly.
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Flaviviruses comprise a genus of viruses that pose a significant burden on human health worldwide. Transmission by both mosquito and tick vectors, and broad host tropism contribute to the presence of flaviviruses globally. Like all viruses, they require utilization of host molecular machinery to facilitate their replication through physical interactions.

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Dengue virus (DENV) disruption of the innate immune response is critical to establish infection. DENV non-structural protein 5 (NS5) plays a central role in this disruption, such as antagonism of STAT2. We recently found that DENV serotype 2 (DENV2) NS5 interacts with Polymerase associated factor 1 complex (PAF1C).

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