By distributing receptor-binding and receptor-destroying proteins asymmetrically on their surface, filamentous influenza A virus particles create a Brownian ratchet that facilitates their passage through mucus.

Rab7-mediated changes in goblet cell function play a crucial role in triggering gut inflammation during colitis.

The hagfish slime glands, which produce a large volume of defensive slime within 0.4 s by ejecting threads and mucus into seawater, evolved from cells and genes expressed in the skin.

Chi3l1 binds to bacterial peptidoglycan, helping anchor and organize bacteria within the mucus layer.

The chloride channel Ano1/Tmem16a plays an essential and non-redundant role in the developing airway by inhibiting mucus cell hyperplasia and promoting proper immune function of the airway mucosal barrier.

Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

The reduction of bicarbonate secretion into the airways reproduces cystic fibrosis-like features, independently of chloride secretion.

Goblet cells use distinct receptors and signaling pathways to independently perform mucus secretion and endocytosis of fluid-phase cargo with atypical trafficking to deliver lumenal substances to the immune system.

KChIP3 localisation by intracellular calcium oscillations controls mucin release from colonic goblet cells.

Contact with bacteria and subsequent hypoxia promotes functional maturation of the immature gastrointestinal tract.