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Compositional changes alter actin binding by phase separated T cell signaling clusters, enabling cluster movement by distinct actin networks.

Autophagy is critical for the turnover of inflammatory signaling complexes containing RHIM-domain proteins.

Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.

Absolute quantification of cohesin, CTCF, NIPBL, WAPL and sororin in HeLa cells implies that some genomic cohesin and CTCF enrichment sites are unoccupied at any one time.

Thermal injury and infected wounds induce distinct inflammatory and remodeling mechanisms that alter the dynamics of wound repair.

VRAC activation, observed with a FRET sensor of intracellular LRRC8-domains movement during gating and by fluorometry, requires plasma membrane localization and diacylglycerol signaling, but is independent of intracellular ionic strength.

Heme-dependent feedback inhibition of rate-limiting ALA-synthesis of plant tetrapyrrole biosynthesis depends on binding of heme to glutamyl-tRNA reductase-binding protein.

Hair cell survival and mitochondrial function is supported by an extracellular stimulator of IGF1 signaling, the protease pregnancy-associated plasma protein-aa.

Recruitment of HOPS tethering complex to target membranes to promote vesicle fusions requires proper complex assembly and specific small GTPases, and HOPS is not transformed from the related miniCORVET complex.

Super-resolution imaging reveals that the microtubule-associated protein Tau regulates the Fyn kinase organisation in dendrites, and that the frontotemporal dementia mutant Tau promotes aberrant Fyn clustering, potentially leading to synaptic dysfunction.