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James Nathan is a researcher at the Cambridge Stem Cell Institute, focusing on cellular mechanisms of oxygen metabolite sensing. His work examines how chromatin modifications are vital for cells to adapt to varying local oxygen and nutrient environments. He aims to uncover how oxygen-sensing pathways impact cell-fate decisions through epigenetic modifications and transcriptional activity. Nathan's research utilizes genome-wide mutagenesis screens and metabolic assays to delve into oxygen-sensitive transcriptional pathways and their implications for cell function. A significant aspect of his current research includes understanding how chromatin marks are selectively modified in response to changes in metabolite oxygen levels, particularly through the identification of hypoxic recruitment of the SET1B histone methyltransferase in chromatin regulation. His work contributes to insights into the fundamental cellular responses to oxygen availability and the mechanisms governing the HIF response at the chromatin level.
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