Publications by authors named "M A Mackey"

Deficits in IL-2 signaling can precipitate autoimmunity by altering the function and survival of FoxP3+ regulatory T cells (Tregs) while high concentrations of IL-2 fuel inflammatory responses. Recently, we showed that the non-beta IL-2 SYNTHORIN molecule SAR444336 (SAR'336) can bypass the induction of autoimmune and inflammatory responses by increasing its reliance on IL-2 receptor α chain subunit (CD25) to provide a bona fide IL-2 signal selectively to Tregs, making it an attractive approach for the control of autoimmunity. In this report, we further demonstrate that SAR'336 can support non-beta IL-2 signaling in murine Tregs and limit NK and CD8+ T cells' proliferation and function.

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The bioaccumulation of polyvinylpyrrolidone-coated silver nanoparticles (PVP-AgNPs) in Palmaria palmata and Ulva sp. seaweed was investigated by ICP-MS and SP-ICP-MS (determination of nanoparticles and size distribution after an enzymatic extraction). Seaweeds were exposed to 0.

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Enzymes that oxidize aromatic substrates have shown utility in a range of cell-based technologies including live cell proximity labeling (PL) and electron microscopy (EM), but are associated with drawbacks such as the need for toxic HO. Here, we explore laccases as a novel enzyme class for PL and EM in mammalian cells. LaccID, generated via 11 rounds of directed evolution from an ancestral fungal laccase, catalyzes the one-electron oxidation of diverse aromatic substrates using O instead of toxic HO, and exhibits activity selective to the surface plasma membrane of both living and fixed cells.

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Purpose Studies regarding the relationship between age-related macular degeneration (AMD) and diabetic retinopathy (DR) conflict: while some support that AMD is protective against DR, others find the opposite. The mechanism by which AMD may protect against DR is unclear. We sought to assess the association between AMD and DR when controlling for glycemic control in patients with diabetes mellitus (DM) type II.

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Glioblastoma (GBM) is a highly malignant and devastating brain cancer characterized by its ability to rapidly and aggressively grow, infiltrating brain tissue, with nearly universal recurrence after the standard of care (SOC), which comprises maximal safe resection followed by chemoirradiation (CRT). The metabolic triggers leading to the reprogramming of tumor behavior and resistance are an area increasingly studied in relation to the tumor molecular features associated with outcome. There are currently no metabolomic biomarkers for GBM.

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