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Given previous demonstrations of how bacterial glycans mediate host immune recognition and response, from host recognition of lipopolysaccharide and peptidoglycan by pattern recognition receptors (e.g., Toll-like receptors) to trigger an immune response to bacteria using glycan mimicry to engage immune tolerance receptors (e.g., DC-SIGN) (Alemka et al., 2013

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Consistent with this postulate, NCBP1-HNEylation-driven translation suppression was ablated in SF3A1-depleted cells compared to knockdown-control (Supplementary Fig