The Mitochondrial Voltage-Dependent Anion Channel 1, Ca Transport, Apoptosis, and Their Regulation.

In the outer mitochondrial membrane, the voltage-dependent anion channel 1 (VDAC1) functions in cellular Ca homeostasis by mediating the transport of Ca in and out of mitochondria. VDAC1 is highly Ca-permeable and modulates Ca access to the mitochondrial intermembrane space. Intramitochondrial Ca controls energy metabolism by enhancing the rate of NADH production modulating critical enzymes in the tricarboxylic acid cycle and fatty acid oxidation.

Two tarantula venom peptides as potent and differential Na(V) channels blockers.

Voltage dependent sodium (Na(V)) channels are large membrane spanning proteins which lie in the basis of action potential generation and propagation in excitable cells and hence are essential mediators of neuronal signaling. Inhibition of Na(V) channel activity is one of the core mechanisms to treat conditions related to neuronal hyperexcitability, such as epilepsy in the clinic. Na(V) channel blockers are also extensively used to locally inhibit action potential generation and related pain perceptions in the form of local anesthetics.

Using antibodies against P2Y and P2X receptors in purinergic signaling research.

The broad expression pattern of the G protein-coupled P2Y receptors has demonstrated that these receptors are fundamental determinants in many physiological responses, including neuromodulation, vasodilation, inflammation, and cell migration. P2Y receptors couple either G(q) or G(i) upon activation, thereby activating different signaling pathways. Ionotropic ATP (P2X) receptors bind extracellular nucleotides, a signal which is transduced within the P2X protein complex into a cation channel opening, which usually leads to intracellular calcium concentration elevation.

Kinetics and Gbetagamma modulation of Ca(v)2.2 channels with different auxiliary beta subunits.

Modulation of calcium channels by both auxiliary subunits and G proteins was studied in cell-attached patches from COS-7 cells transfected with Ca(v)2.2 channel subunits (N-type, alpha(1)B and either beta(1b) or beta(2a)). These were co-expressed with either Gbeta(1)gamma(2) or the Gbetagamma-binding domain of beta-adrenergic-receptor kinase-1 to sequester endogenous Gbetagamma.

The ducky mutation in Cacna2d2 results in altered Purkinje cell morphology and is associated with the expression of a truncated alpha 2 delta-2 protein with abnormal function.

The mouse mutant ducky, a model for absence epilepsy, is characterized by spike-wave seizures and cerebellar ataxia. A mutation in Cacna2d2, the gene encoding the alpha 2 delta-2 voltage-dependent calcium channel accessory subunit, has been found to underlie the ducky phenotype. The alpha 2 delta-2 mRNA is strongly expressed in cerebellar Purkinje cells.