Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.

Personalized heart muscle cells made from stem cells in the laboratory could be used to check an individual’s response to potential new drugs before clinical trials.

The fusion of astronomy and cellular cardiology reveals the 3D arrangement and the firing reliability of active excitation-contraction coupling sites in beating cardiac myocytes.

Electrophysiological and simulation approaches show that a chloride-related longer relaxation of the inhibitory synaptic events partially compensates the early defect in the chloride homeostasis detected in fetal SOD spinal motoneurons.

Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.

A cationic molecule derived from an uncharged Cav2.2 calcium channel inhibitor powerfully inhibits both sodium and calcium channels with extracellular application and inhibits both pain and neurogenic inflammation.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.

A family of fluorescent biosensors for nicotinamide adenine dinucleotides allows quantification of these cofactors in live cells with spatio-temporal resolution.

At mitosis, NuMA recruits dynein-dynactin to microtubule minus-ends, enabling robust microtubule clustering and the emergence of spindle poles.

Interaction of P. falciparum with the erythrocyte activates a phosphorylation cascade altering the viscoelastic properties of this area of the host membrane conditioning it for successful invasion.