Results 281 to 290 of about 242,791 (386)

Somatostatin modulation of initial fusion pores in Ca2+‐triggered exocytosis from mouse chromaffin cells

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Somatostatin binds to a G‐protein‐coupled receptor to inhibit the release of catecholamine from chromaffin cells. This action has no impact on Ca2+ levels and is similar for Ca2+ entry through voltage‐gated Ca2 channels and for Ca2+ mobilization from the endoplasmic reticulum.
Jinbo Cheng, Meyer B. Jackson
wiley   +1 more source

Glial cells in the heart: Implications for their roles in health and disease

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic representation of cardiac autonomic ganglia within epicardial fat pads (posterior heart surface shown), containing vagal postganglionic neuron cell bodies, associated fibres, and glia. These ganglia receive cholinergic input from vagal preganglionic neurons and adrenergic input from sympathetic postganglionic neurons ...
Svetlana Mastitskaya   +2 more
wiley   +1 more source

Structure mirroring function: What's the ‘matter’ with the funny current?

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The ‘funny’ (If) current of cardiac pacemaker cells has been first identified in the late 1970s as a major mechanism in the generation and control of cardiac pacemaking. Decades of studies have since described the properties of the funny current and of its molecular components, HCN channels, in the heart and brain, providing the ...
Andrea Saponaro, Dario DiFrancesco
wiley   +1 more source

Catecholaminergic polymorphic ventricular tachycardia–linked ryanodine receptor variants exhibit domain‐specific calcium leak and calmodulin affinity properties

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Catecholaminergic polymorphic ventricular tachycardia (CPVT) variants in N terminal (NTD) and central domain (CD) but not pore domain induce a pathological RyR2 conformational shift upon protein kinase A (PKA) phosphorylation, similar to that seen in heart failure (HF), calcium/calmodulin‐dependent protein kinase II (CaMKII ...
Hitoshi Uchinoumi   +11 more
wiley   +1 more source

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