Titlebook: Intracellular Regulation of Ion Channels; Martin Morad,Zalman Agus Conference proceedings 1992 Springer-Verlag Berlin Heidelberg 1992 ATP.

補(bǔ)角

Tissue distribution and possible function of the subunits of the L-type calcium channelsssential for EC-coupling in skeletal muscle. The transverse tubular membrane of skeletal muscle contains a high density of the calcium channel protein, the so called receptor for calcium channel blockers (CaCB-receptor) [1]. The charge moved during excitation-contraction coupling (EC-coupling) is lo

Folklore

expunge

sperse

Membrane-Delimited Stimulation of Heart Cell Calcium Current by ?-Adrenergic Signal-Transducing Gs Phanced adenosine 3’,5’-cyclic monophosphate (cAMP)dependent phosphorylation of calcium (Ca) channels following .-receptor activation of the guanosine nucleotide-binding (G) protein Gs, and Gs-activation of the adenylyl cyclase cascade. We blocked phosphorylation pathways in guinea pig ventricular ca

Prostatism

Participation of a Fast G Protein Pathway in the ?-Adrenergic Regulation of Cardiac Calcium Channelshis increase is generally attributed to ?-adrenergic receptor-stimulated cAMP-dependent phosphorylation of the Ca channel (Hartzell, 1988; Trautwein & Hescheler, 1990). Recently, it has been suggested that cAMP-dependent phosphorylation cannot explain all the effects of ?-adrenergic agonists on I. a

搏斗

Kinetics of a G-Protein Mediated Action on Neuronal Ca2+ Channelsvement of GTP-binding proteins in the inhibitory modulation of Ca channel is usually supported by one or more of the following observations: (1) The non-hydrolysable GTP analogue, GTPγS, reproduces the inhibitory action of external neurotransmitters (Dolphin and Scott, 1987), (2) Ca channel modulati

極微小

Ambulatory

工作

The Na+-Activated K+ Channel in Cardiac Cellsby the inrushing Na. ions during the upstroke of the action potential. More recently the experimental evidence for this thesis has been criticized by Dryer (1991). In heart the channel was regarded to play only a role in pathophysiological conditions of Na.,K. pump blockade by digitalis.

Adjourn

Tissue distribution and possible function of the subunits of the L-type calcium channelscated in the CaCB-receptor and can be blocked by dihydropyridines and phenylalkylamines [2]. It is likely that in skeletal muscle the CaCB-receptor functions only as voltage sensor and not as calcium conducting channel since EC-coupling does not require calcium entry in skeletal muscle.