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Robert Saxton

disease excessive inflammation can damage bystander tissues compromise biological function. To prevent this mammals have evolved a complex array of signaling molecules receptors that ensure the protection repair of host tissues. However failure of these homeostatic systems can result

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Robert Saxton is an Assistant Professor of Immunology and Molecular Medicine at the University of California, Berkeley, in the Department of BIO. His research focuses on the mechanisms of cell communication that control tissue inflammation, repair, and homeostasis, with the goal of developing novel therapeutics to modulate these pathways in disease. His work explores the signaling mechanisms that enable the resolution of inflammation, immune-mediated tissue repair, and the role of metabolic signals in immune function. Saxton's research employs biochemical and structural biology techniques, along with protein engineering and mouse models, to understand and control inflammatory signaling at multiple levels.


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Robert A. Saxton is a researcher at UC Berkeley with expertise in Immunology, Cell signaling, and Protein engineering. His work focuses on understanding the molecular mechanisms underlying mTOR signaling, particularly its role in growth, metabolism, and disease. Saxton's research explores how proteins such as Sestrin2, CASTOR, and SAMTOR function as sensors for amino acids and other nutrients, regulating the mTORC1 pathway. He also investigates cytokine receptor signaling, including the structural basis of Janus kinase activation and the therapeutic potential of cytokine adaptors. His studies aim to uncover how immune signaling can be redirected for therapeutic applications.

Source: google_scholar · 96 words
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