The Peptide Components of Bee Venom

Gauldie, Jack; Hanson, Jennifer M.; Rumjanek, Franklin David; Shipolini, Rudolf A.; Vernon, C. A.

doi:10.1111/j.1432-1033.1976.tb10030.x

Cited by 199 publications

(110 citation statements)

References 30 publications

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“…The ionophore A23 187 (Calbiochem, La Jolla CA) was dissolved in dimethylsulfoxide, which was added to both control and test media at final concentrations not exceeding 0.1% (v/v). Apamin, purified as in [20] was kindly provided by Dr M. Lazdunski (Centre de Biochimie, CNRS, Nice). All results are expressed as mean value (k SEM) together with the number of individual determinations (n).…”

Section: Introduction 2 Materials and Methodsmentioning

confidence: 99%

Resistance to apamin of the Ca²⁺‐activated K⁺ permeability in pancreatic B‐cells

et al. 1983

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The bee venom neurotoxin apamin failed to affect 86Rb outflow and insulin release from rat pancreatic islets stimulated by D-glucose or the Ca2' -ionophore A23 187. Apamin, in contrast to quinine or A23 187, also failed to affect bioelectrical activity in mouse islet cells. These findings suggest that, like in erythrocytes, and at variance with the situation found in smooth muscle, liver or neuroblastoma cells, the Ca2+-activated K+ permeability in the pancreatic B-cell is resistant to apamin. Pancreatic islet cellCa2+-activated permeability Auamin Insulin release Electrical activity _

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Section: Introduction 2 Materials and Methodsmentioning

confidence: 99%

Resistance to apamin of the Ca²⁺‐activated K⁺ permeability in pancreatic B‐cells

et al. 1983

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“…Melittin-phospholipid interactions have also been extensively studied [3-51, however few studies have been dealing with the structure of the peptide itself, in solution. It is known to behave as a tetramer [ 1,6]; it is also assumed from an early circular dichroism study [7] to be mainly in random coil. The possibility of conformational and aggregation changes induced by organic solvent or phospholipids was pointed out [8,9] but no definite experimental proof was presented on these problems.…”

Section: Introductionmentioning

confidence: 99%

Conformational change and self association of monomeric melittin

Talbot¹,

Dufourcq²,

Bony³

et al. 1979

FEBS Letters

199

128

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“…We have examined the role of S1P 1 and I K ACh in the observed decrease in myocyte shortening by taking advantage of the availability of a specific blocker for the inwardly rectifying K ϩ channel that is linked to the M 2 and the S1P receptors in adult heart. One such compound is tertiapin, a small peptide (21 amino acids) purified from the venom of honey bees (15). Tertiapin selectively blocks I K ACh in cardiac myocytes by acting on the extracellular surface of this K ϩ channel (13,25,54).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of the negative inotropic effects of sphingosine-1-phosphate on adult mouse ventricular myocytes

Landeen

Dederko²,

Kondo³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Landeen LK, Dederko DA, Kondo CS, Hu BS, Aroonsakool N, Haga JH, Giles WR. Mechanisms of the negative inotropic effects of sphingosine-1-phosphate on adult mouse ventricular myocytes. Am J Physiol Heart Circ Physiol 294: H736-H749, 2008. First published November 16, 2007 doi:10.1152/ajpheart.00316.2007.-Sphingosine-1-phosphate (S1P) induces a transient bradycardia in mammalian hearts through activation of an inwardly rectifying K ϩ current (IK ACh ) in the atrium that shortens action potential duration (APD) in the atrium. We have investigated probable mechanisms and receptor-subtype specificity for S1P-induced negative inotropy in isolated adult mouse ventricular myocytes. Activation of S1P receptors by S1P (100 nM) reduced cell shortening by ϳ25% (vs. untreated controls) in fieldstimulated myocytes. S1P 1 was shown to be involved by using the S1P 1-selective agonist SEW2871 on myocytes isolated from S1P3-null mice. However, in these myocytes, S1P 3 can modulate a somewhat similar negative inotropy, as judged by the effects of the S1P 1 antagonist VPC23019. Since S1P1 activates Gi exclusively, whereas S1P 3 activates both Gi and Gq, these results strongly implicate the involvement of mainly G i. Additional experiments using the IK ACh blocker tertiapin demonstrated that IK ACh can contribute to the negative inotropy following S1P activation of S1P 1 (perhaps through Gi␤␥ subunits). Mathematical modeling of the effects of S1P on APD in the mouse ventricle suggests that shortening of APD (e.g., as induced by I K ACh ) can reduce L-type calcium current and thus can decrease the intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) transient. Both effects can contribute to the observed negative inotropic effects of S1P. In summary, these findings suggest that the negative inotropy observed in S1P-treated adult mouse ventricular myocytes may consist of two distinctive components: 1) one pathway that acts via G i to reduce L-type calcium channel current, blunt calcium-induced calcium release, and decrease [Ca 2ϩ ]i; and 2) a second pathway that acts via Gi to activate IK ACh and reduce APD. This decrease in APD is expected to decrease Ca 2ϩ influx and reduce [Ca 2ϩ ]i and myocyte contractility.calcium; contraction; cell shortening; inhibitory G protein; acetylcholine-sensitive potassium; myocyte SPHINGOSINE-1-PHOSPHATE (S1P) is a biologically active, cell membrane-associated sphingolipid that binds with high affinity to five distinct G-coupled protein receptor isoforms (S1P 1-5 ). S1P 1 has been detected in abundance in neonatal rat cardiomyocytes (39). In these cells, exposure to S1P (500 nM) results in an initial negative inotropic effect (reduction of systolic calcium). However, this may be followed by calcium overload (increased diastolic calcium) and then a cessation of contractility. In isolated atrial myocytes, S1P has been shown to activate a weakly inwardly rectifying potassium (K ϩ ) current. This K ϩ conductance is very similar to the K ϩ current activated by ACh (I K ACh ). Activation of this current can shorte...

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The Peptide Components of Bee Venom

Cited by 199 publications

References 30 publications

Resistance to apamin of the Ca²⁺‐activated K⁺ permeability in pancreatic B‐cells

Resistance to apamin of the Ca²⁺‐activated K⁺ permeability in pancreatic B‐cells

Conformational change and self association of monomeric melittin

Mechanisms of the negative inotropic effects of sphingosine-1-phosphate on adult mouse ventricular myocytes

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The Peptide Components of Bee Venom

Cited by 199 publications

References 30 publications

Resistance to apamin of the Ca2+‐activated K+ permeability in pancreatic B‐cells

Resistance to apamin of the Ca2+‐activated K+ permeability in pancreatic B‐cells

Conformational change and self association of monomeric melittin

Mechanisms of the negative inotropic effects of sphingosine-1-phosphate on adult mouse ventricular myocytes

Contact Info

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Resistance to apamin of the Ca²⁺‐activated K⁺ permeability in pancreatic B‐cells

Resistance to apamin of the Ca²⁺‐activated K⁺ permeability in pancreatic B‐cells