Chronic perturbations of spiking activity trigger compensatory changes in GABAergic synaptic strength, but not compensatory changes in AMPAergic synaptic strength.

TBX5-loss associated cardiomyocyte ectopy and atrial fibrillation is prevented by augmentation of SERCA2 activity, establishing a mechanism underlying the genetic basis for a Ca²⁺-dependent pathway for AF risk.

Activation of CaMKII holoenzymes triggers the exchange of subunits with other holoenzymes, including unactivated ones, enabling the calcium-independent phosphorylation and activation of new subunits.

Mesoscale cortical calcium activity correlating with single cortical and thalamic cell spiking reveal rich dynamics and support a novel approach for investigating in vivo functional networks in the mammalian brain.

Triggered activity bursts in place cells can increase and decrease the strength of some inputs.

The phosphorylation of FLS2 may activate flg22-triggered immunity by facilitating the partitioning of FLS2 into functional AtRem1.3-associated nanodomains.

The transcription factor bZIP63 is a key regulator of the starvation response in the model plant Arabidopsis thaliana and is directly targeted by the kinase SnRK1.

Atomic force microscopy based single-molecule force spectroscopy of smooth muscle myosin light chain kinase strongly indicates the existence of a mechanically triggerable activation pathway analogous to its well-established biochemical regulation pathway via calcium-loaded calmodulin.

Biologically plausible changes in the excitabilities of single neurons may suffice to selectively modulate sequential network dynamics, without modifying of recurrent connectivity.