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Calcium -dependent K+ channel

Ghisdal, P., and Morel, N. 2001. Cellular target of voltage and calcium-dependent K+ channel blockers involved in EDHF-mediated responses in rat superior mesenteric artery. Br. J. Pharmacol. 134 1021-1028. [Pg.372]

Sauve, R., Parent, L., Simoneau, C., and Roy, G. 1988. External ATP triggers a biphasic activation process of a calcium-dependent K+ channel in cultured bovine aortic endothelial cells. Pflugers Arch. 41 469—481. [Pg.373]

In addition to intracellular heme-containing proteins, big-conductance calcium-dependent K+ (BKCa) channels and calcium-spark activated transient Kca channels in plasma membrane are also tar geted by CO [3]. As well known, nitric oxide (NO) also activates BKca channels in vascular smooth muscle cells. While both NO and CO open BKCa channels, CO mainly acts on alpha subunit of BKCa channels and NO mainly acts on beta subunit of BKca channels in vascular smooth muscle cells. Rather than a redundant machinery, CO and NO provide a coordinated regulation of BKca channel function by acting on different subunits of the same protein complex. Furthermore, pretreatment of vascular smooth muscle... [Pg.322]

Krasnoperov VG, Beavis R, Chepumy OG et al (1996) The calcium-independent receptor of a-latrotoxin is not a neurexin. Biochem Biophys Res Commun 227 868-75 Krasnoperov VG, Bittner MA, Beavis R et al (1997) a-Latrotoxin stimulates exocytosis by the interaction with a neuronal G-protein-coupled receptor. Neuron 18 925-37 Krasnoperov VG, Bittner MA, Mo W et al (2002b) Protein tyrosine phosphatase-G is a novel member of the functional family of a-latrotoxin receptors. J Biol Chem 277 35887-95 Kreienkamp HJ, Zitzer H, Gundelfinger ED et al (2000) The calcium-independent receptor for a-latrotoxin from human and rodent brains interacts with members of the ProSAP/SSTRIP/Shank family of multidomain proteins. J Biol Chem 275 32387-90 Lajus S, Lang J (2006) Splice variant 3, but not 2 of receptor protein-tyrosine phosphatase a can mediate stimulation of insulin-secretion by a-latrotoxin. J Cell Biochem 98 1552-9 Lajus S, Vacher P, Huber D et al (2006) a-Latrotoxin induces exocytosis by inhibition of voltage-dependent K+ channels and by stimulation of L-type Ca2+ channels via latrophilin in [5-cells. J Biol Chem 281 5522-31... [Pg.202]

Type II diabetes Stimulating the release of insulin from the pancreas. ATP-dependent K-channel blocker Calcium hydrogen phosphate, MCC, maize starch, polacrilin, potassium, povidone, glycerol (85%), magnesium stearate, meglumine, poloxamer Novo Nordisk... [Pg.14]

With modest increase in intracellular ROS levels, activation of NF-kB takes place, which protects the cell against oxidative stress [45], Direct root of ROS participation in signal transduction from cell membrane to intracellular metabolic reactions were recently described. Among them - activation of potential-dependent K-channels and variation of membrane potential, inhibition of cellular protein phosphatases and restriction of activity of MAP-kinase [49]. Such view on intracellular role of ROS consider them as second messengers, which together with cyclic nucleotides, calcium ions, and other biologically active compounds provides adequate cell response to the outer signals. [Pg.162]

From the earliest measurements of tissue calcium, it was clear that total calcium is largely a measure of stored calcium. Through the years, scientists have used a variety of indirect measures of [Ca2+]j. These include shortening of or tension in muscles secretion from secretory cells the activity of Ca2+-dependent enzymes, most notably glycogen phosphorylase and flux of K+, or K+ currents, as a reflection of Ca2+-activated K+ channels. In addition, investigators often use the radioactive calcium ion [45Ca2+] as an indirect indicator of Ca2+ concentrations and Ca2+ movements. [Pg.379]

Fig. 4.1. Cellular model illustrating cell types in vascular wall involved in vasorelaxation induced by SERMs. Putative targets of SERMs are indicated within cyan tags. SERMs directly affect L-type VDCC, BK fil subunit in smooth muscle cells, and ER in endothelial cells. L-type VDCC L-type voltage-dependent calcium channel BK calcium-activated large conductance K+ channel PKG protein kinase G eNOS endothelial nitric oxide synthase GC soluble guanylate cyclase cGMP cyclic GM P V electrochemical membrane potential ER estrogen receptor. See text for further details... Fig. 4.1. Cellular model illustrating cell types in vascular wall involved in vasorelaxation induced by SERMs. Putative targets of SERMs are indicated within cyan tags. SERMs directly affect L-type VDCC, BK fil subunit in smooth muscle cells, and ER in endothelial cells. L-type VDCC L-type voltage-dependent calcium channel BK calcium-activated large conductance K+ channel PKG protein kinase G eNOS endothelial nitric oxide synthase GC soluble guanylate cyclase cGMP cyclic GM P V electrochemical membrane potential ER estrogen receptor. See text for further details...
Creed KE, Ishikawa S, Ito Y 1983 Electrical and mechanical activity recorded from rabbit urinary bladder in response to nerve stimulation. J Physiol 338 149-164 Cui J, Cox DH, Aldrich RW 1997 Intrinsic voltage dependence and Ca2+ regulation of mslo large conductance Ca-activated K+ channels. J Gen Physiol 109 647-673 Fabiato A 1983 Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am J Physiol 245 0-04... [Pg.202]

Adams PJ, Garcia E, Mulatz K, Spacey SD, Snutch TP (2006) Familial Hemiplegic Migraine Mutation K1336E Differentially Affects Calcium-Dependent Facilitation Of P/Q-Type Calcium Channel Splice Variants. FENS Forum Abstracts vol. 3 A084.082. [Pg.244]

Genistein (42) was found to affect many other types of channels, but the main proposed mechanism of these interactions was indirect. In most cases a PTK pathway was suggested as a putative explanation of the observed effects. Since genistein (42) is a well-known inhibitor of this kinase, we will not focus on those papers and only a short list will be presented. Such a mechanism was mentioned in the case of inhibition of ATP-sensitive K+ channels [325], cardiac slowly activating delayed-rectifier K+ current [326], L-type calcium channels [327,328] (contrary to the direct interaction proposed by Chiang et al. [306] and Yokoshiki et al. [307]), P/Q-type calcium channels in rat hippocampal neurons [329], and carotid baroreceptor activity [330]. A PTK-dependent mechanism was also proposed as the explanation of potentiation of neuronal a7 nAGhRs by genistein (42) [331]. [Pg.292]


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