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Machine learning-assisted experiments reveal CD81 as a novel binding partner of CD44 in driving cancer stemness, tumor cell clustering, and extracellular vesicle integrity in human and mouse breast cancer.

A novel conditional mouse model to interrogate the requirements of structure-selective endonucleases in the development, functionality, and genome stability of B lymphocytes.

A combination of single molecule fluorescence with DMD simulations and disulfide mapping resolved the multistate structural landscape of the PSG supramodule from PSD-95, which explains how interdomain interactions within PSD-95 enable PDZ3 binding of the critical synaptic adhesion protein neuroligin.

A set of canonical computational principles implemented in a simple feedforward neural network naturally gives rise to the network's sensitivity to numerosity and its illusory effects, providing an explanation for the ubiquity of the number sense in the animal kingdom.

The priming protein ubMunc13-2 and Synaptotagmin-7 cooperate with phorbolesters/diacylglycerol to stimulate vesicle priming in adrenal chromaffin cells, whereas phorbolesters/diacylglycerol interacting with Munc13-1 inhibit vesicle fusion, which identifies opposing functions of these two Munc13 proteins.

A combination of unbiased scRNA-sequencing and functional approaches in organoid cultures and injury-repair models in vivo reveals major heterogeneity in adult murine airway basal cells, which is established prenatally and conserved in humans.

A comprehensive meta-analysis of the neuroimaging literature reveals that the lateral prefrontal cortex of humans is mainly organized along its rostrocaudal axis according to a unimodal-to-transmodal pattern of network connectivity and a concrete-to-abstract axis of functional associations.

The interaction between rDNA instability and proteostasis stress, two major aging hallmarks, underlies single-cell aging trajectories in yeast.

Endothelial sphingolipid biosynthesis is essential for maintaining vascular development, neovascular proliferation, non-CNS tissue sphingolipid levels, and hepatocyte response to stress.

Experimental evolution of yeast models of congenital disorders of glycosylation reveals that reduction, but not loss, of phosphoglucomutase activity best compensates for impaired phosphomannomutase activity.