Mucins, long associated with cancer aggression, remodel the cancer glycocalyx in a way that promotes proliferation in the metastatic site by enhancing integrin-mediated adhesion and thus driving cell cycle progression.
Impaired autophagy influences intestinal inflammation and hypersensitivity responses by orchestrating mucosal T cell populations, suggesting new translational perspectives for the treatment of these conditions.
Transcriptome analysis reveals an alternative splicing program induced in the arterial endothelium under low-flow inflammatory conditions by platelet and macrophage recruitment and dependent upon the RNA-binding splice factor Rbfox2.
Immune expulsion of helminth parasites is driven by two key pathways mediated by soluble cytokines ligating to the IL-4 and IL-25 receptors acting on innate effector cells throughout the course of infection.
Structures of RNA polymerase I transcription machinery revealed a ratcheting motion within the complex in coordination with three distinct functional states, implicating a novel mechanism for promoter bubble opening in the absence of ATP hydrolysis.