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In this study, the central mechanism underlying TAM lipid metabolic reprogramming relies on NP-mediated targeted siCB-2 delivery to TAMs, which silences CB-2 expression, disrupts the 2-AG signaling cascade, and redirects TAM polarization toward the pro-inflammatory M1 phenotype, ultimately restoring anti-tumor immune responses

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Lysates containing the tagged-DDX3X were enriched for GS-DDX3X using IgG Sepharose 6 Fast Flow affinity resins (GE Healthcare)

This suggests a reduced need for cytoskeletal kinase activity 81 and apolipoprotein A-1 binding related to fat transport 82 , potentially as a response to altered metabolic demands by enrichment

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