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β-Pompilidotoxin Sale

(Synonyms: Arg-Ile-Lys-Ile-Gly-Leu-Phe-Asp-Gln-Leu-Ser-Arg-Leu ) 目录号 : GP10111

β-Pompilidotoxin (β-PMTX),一种黄蜂毒液,可以减缓钠通道失活并增加细胞中的稳态钠电流。

β-Pompilidotoxin Chemical Structure

Cas No.:216064-36-7

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1mg
¥305.00
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5mg
¥903.00
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10mg
¥1,523.00
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25mg
¥2,153.00
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产品描述

β-Pompilidotoxin, (C71H124N22O17), a peptide with the sequence H2N-Arg

-Ile-Lys-Ile-Gly-Leu-Phe-Asp-Gln-Leu-Ser-Arg-Leu-amide, MW= 1557.88. Pompilidotoxin is a toxin from the venom of spider wasps that slows the inactivation of Na+channels. α-Pompilidotoxin (α-PMTX) can be extracted from the venom of a solitary wasp, Anopolis samariensis. β-Pompilidotoxin (β-PMTX) originates from the venom of another wasp, Batozonellus maculifrons(1). Homology α-PMTX has no structural homology with other toxins. It lacks disulfide bonds which are known to be present in other toxins acting on sodium channels, such as sea anemone toxins or scorpion toxins(2). Both α- and β-PMTX slow the inactivation of neuronal sodium channels (but not heart sodium channels), possibly by binding to the neurotoxin receptor site 3 on the extracellular surface of the sodium channel(3). β-PMTX has higher potency than α-PMTX. By slowing down the inactivation of sodium channels, PMTXs can potentiate synaptic transmission in the lobster neuromuscular endplate.

References:
1. Konno K, Hisada M, Itagaki Y, Naoki H, Kawai N, Miwa A, Yasuhara T, Takayama H (1998). "Isolation and structure of pompilidotoxins, novel peptide neurotoxins in solitary wasp venoms". Biochem Biophys Res Commun. 250 (3): 612–6.
2. Sahara Y, Gotoh M, Konno K, Miwa A, Tsubokawa H, Robinson HP, Kawai N (2000). "A new class of neurotoxin from wasp venom slows inactivation of sodium current". Eur J Neurosci. 12 (6): 1961–70.
3. Kawai N, Konno K (2004). "Molecular determinants of two neurotoxins that regulate sodium current inactivation in rat hippocampal neurons". Neurosci Lett. 361 (1-3): 44–6.

 

Chemical Properties

Cas No. 216064-36-7 SDF
别名 Arg-Ile-Lys-Ile-Gly-Leu-Phe-Asp-Gln-Leu-Ser-Arg-Leu
化学名 β-Pompilidotoxin
Canonical SMILES CCC(C)C(C(=O)NC(CCCCN)C(=O)NC(C(C)CC)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CC1=CC=CC=C1)C(=O)NC(CC(=O)O)C(=O)NC(CCC(=O)N)C(=O)NC(CC(C)C)C(=O)NC(CO)C(=O)NC(CCCN=C(N)N)C(=O)NC(CC(C)C)C(=O)N)NC(=O)C(CCCN=C(N)N)N
分子式 C71H124N22O17 分子量 1557.9
溶解度 ≥ 155.8mg/mL in DMSO 储存条件 Desiccate at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 0.6419 mL 3.2094 mL 6.4189 mL
5 mM 0.1284 mL 0.6419 mL 1.2838 mL
10 mM 0.0642 mL 0.3209 mL 0.6419 mL
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Research Update

β-pompilidotoxin modulates spontaneous activity and persistent sodium currents in spinal networks

The origin of rhythm generation in mammalian spinal cord networks is still poorly understood. In a previous study, we showed that spontaneous activity in spinal networks takes its origin in the properties of certain intrinsically spiking interneurons based on the persistent sodium current (INaP). We also showed that depolarization block caused by a fast inactivation of the transient sodium current (INaT) contributes to the generation of oscillatory activity in spinal cord cultures. Recently, a toxin called Beta-pompilidotoxin (β-PMTX) that slows the inactivation process of tetrodotoxin (TTX)-sensitive sodium channels has been extracted from the solitary wasp venom. In the present study, we therefore investigated the effect of β-PMTX on rhythm generation and on sodium currents in spinal networks. Using intracellular recordings and multielectrode array (MEA) recordings in dissociated spinal cord cultures from embryonic (E14) rats, we found that β-PMTX reduces the number of population bursts and increases the background asynchronous activity. We then uncoupled the network by blocking all synaptic transmission (APV, CNQX, bicuculline and strychnine) and observed that β-PMTX increases both the intrinsic activity at individual channels and the number of intrinsically activated channels. At the cellular level, we found that β-PMTX has two effects: it switches 58% of the silent interneurons into spontaneously active interneurons and increases the firing rate of intrinsically spiking cells. Finally, we investigated the effect of β-PMTX on sodium currents. We found that this toxin not only affects the inactivation of INaT but also increases the peak amplitude of the persistent sodium current (INaP). Altogether, theses findings suggest that β-PMTX acting on INaP and INaT enhances intrinsic activity leading to a profound modulation of spontaneous rhythmic activity in spinal networks.

Structure-Activity Relationship Evaluation of Wasp Toxin β-PMTX Leads to Analogs with Superior Activity for Human Neuronal Sodium Channels

Beta-pompilidotoxin (β-PMTX) is a 13-amino acid wasp venom peptide that activates human neuronal sodium channel NaV1.1 with weak activity (40% activation at 3.3 μM of β-PMTX). Through rational design of β-PMTX analogs, we have identified peptides with significantly improved activity on human NaV1.1 (1170% activation at 3.3 μM of peptide 18). The underlying structure-activity relationship suggests importance of charge interactions (from residue Lys-3) and lipophilic interactions (from residue Phe-7 and Ser-11). Three top-ranked analogs showed parallel activity improvement for other neuronal sodium channels (human NaV1.2/1.3/1.6/1.7) but not muscular subtypes (NaV1.4/1.5). Finally, we found that analog 16 could partially rescue the pharmacological block imposed by NaV1.1/1.3 selective inhibitor ICA-121431 in cultured mouse cortical GABAergic neurons, demonstrating an activating effect of this peptide on native neuronal sodium channels and its potential utility as a neuropharmacological tool.

Production of resurgent current in NaV1.6-null Purkinje neurons by slowing sodium channel inactivation with Beta-pompilidotoxin

Voltage-gated tetrodotoxin-sensitive sodium channels of Purkinje neurons produce "resurgent" current with repolarization, which results from relief of an open-channel block that terminates current flow at positive potentials. The associated recovery of sodium channels from inactivation is thought to facilitate the rapid firing patterns characteristic of Purkinje neurons. Resurgent current appears to depend primarily on NaV1.6 alpha subunits, because it is greatly reduced in "med" mutant mice that lack NaV1.6. To identify factors that regulate the susceptibility of alpha subunits to open-channel block, we voltage clamped wild-type and med Purkinje neurons before and after slowing conventional inactivation with Beta-pompilidotoxin (beta-PMTX). beta-PMTX increased resurgent current in wild-type neurons and induced resurgent current in med neurons. In med cells, the resurgent component of beta-PMTX-modified sodium currents could be selectively abolished by application of intracellular alkaline phosphatase, suggesting that, like in NaV1.6-expressing cells, the open-channel block of NaV1.1 and NaV1.2 subunits is regulated by constitutive phosphorylation. These results indicate that the endogenous blocker exists independently of NaV1.6 expression, and conventional inactivation regulates resurgent current by controlling the extent of open-channel block. In Purkinje cells, therefore, the relatively slow conventional inactivation kinetics of NaV1.6 appear well adapted to carry resurgent current. Nevertheless, NaV1.6 is not unique in its susceptibility to open-channel block, because under appropriate conditions, the non-NaV1.6 subunits can produce robust resurgent currents.