Browse our latest Computational and Systems Biology articles

Killer T cells swarm around tumour targets by accelerating the recruitment of distant T cells, which upon arrival and target engagement augment the chemotactic signal in a positive feedback loop.

The first epigenetic clock for rats was developed and revealed to reflect phenotypic aging and captured the effects of longevity interventions.

Selection for undifferentiated multicellularity emerges in an evolutionary cell-based model because a collective of cells performs chemotaxis better than single cells in a noisy environment.

The physical interaction network encoded in the multi-domain protein native structure handles the trade-off between the fast, stable folding and the efficient, reliable function.

Fully assembled DNA methylomes from phylogeographically diverse clinical Mycobacterium tuberculosis complex isolates reveals 'intercellular mosaic methylation' as a source of epigenetic diversity.

Deep neural networks can be trained to automatically find mechanistic models which quantitatively agree with experimental data, providing new opportunities for building and visualizing interpretable models of neural dynamics.

A massively multiplexed multi-condition screen shows that protein interactomes are larger than previously thought and contain highly dynamic regions that reorganize to drive or respond to cellular changes.

Metabolic activity of the methionine/S-adenosylmethionine cycle is sensed and transcriptionally regulated by a nuclear hormone receptor in Caenorhabditis elegans in order to maintain metabolic homeostasis in a tightly controlled regime.

Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

Regulatory networks of genes controlling different aspects of insect reproduction have been identified by a systems-level analysis of quantitative phenotypic information obtained from the loss of individual cell signaling genes.