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Ubiquitous transcriptional factor-CBP/p300 interaction induces epigenetic and transcriptional bimodality, which can be utilized to tune mean gene expression and noise independently.

Structures of active and inactive conformations of a PP2C family phosphatase reveal a conserved switch that controls enzymatic activity and point to an unexpected relationship between phosphatases and proteasomal proteases.

Metabolic abnormalities in hepatocytes cause the alteration of transcriptional profile and function of immune cells in the tissue microenvironment.

Loss of functional dystroglycan disrupts the formation and function of CCK⁺/CB₁R⁺ inhibitory synapses in hippocampal CA1, resulting in reduced seizure thresholds in mouse models of dystroglycanopathy.

A bacterial CO₂ concentrating mechanism enables Escherichia coli to fix CO₂ from ambient air into biomass.

Single-cell and bulk expression analyses reveal that HCMV latent infection drives cells towards a weaker immune-responsive state, which is important for its expression and reactivation.

Centromeric protein M (CENP-M) is required for the stabilization of a quaternary complex that plays a crucial role in kinetochore organization and function.

Cereblon-based small-molecule degraders rely on the sequential action of ubiquitin-conjugating enzymes UBE2G1 and UBE2D3 to assemble K48-linked polyubiquitin chains on cereblon neomorphic substrates, resulting in their proteasomal degradation.

The combinatorial assembly of different adaptor complexes is a mechanism that dynein uses to interact with multiple cargos.