Peptide neurotoxins from the marine fish-hunting snails of the genus CONUS. They contain 13 to 29 amino acids which are strongly basic and are highly cross-linked by disulfide bonds. There are three types of conotoxins, omega-, alpha-, and mu-. OMEGA-CONOTOXINS inhibit voltage-activated entry of calcium into the presynaptic membrane and therefore the release of ACETYLCHOLINE. Alpha-conotoxins inhibit the postsynaptic acetylcholine receptor. Mu-conotoxins prevent the generation of muscle action potentials. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed)
A genus of cone-shaped marine snails in the family Conidae, class GASTROPODA. It comprises more than 600 species, many containing unique venoms (CONUS VENOMS) with which they immobilize their prey.
Venoms from mollusks, including CONUS and OCTOPUS species. The venoms contain proteins, enzymes, choline derivatives, slow-reacting substances, and several characterized polypeptide toxins that affect the nervous system. Mollusk venoms include cephalotoxin, venerupin, maculotoxin, surugatoxin, conotoxins, and murexine.
Marine, freshwater, or terrestrial mollusks of the class Gastropoda. Most have an enclosing spiral shell, and several genera harbor parasites pathogenic to man.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
Chemical groups containing the covalent disulfide bonds -S-S-. The sulfur atoms can be bound to inorganic or organic moieties.
A covalently linked dimeric nonessential amino acid formed by the oxidation of CYSTEINE. Two molecules of cysteine are joined together by a disulfide bridge to form cystine.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
Processes involved in the formation of TERTIARY PROTEIN STRUCTURE.
An aquatic genus of the family, Pipidae, occurring in Africa and distinguished by having black horny claws on three inner hind toes.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.

Effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline release and purinergic neuroeffector transmission in rat tail artery. (1/206)

1. The effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline (NA) and adenosine 5'-triphosphate (ATP) release from postganglionic sympathetic nerves have been investigated in rat tail arteries in vitro. Intracellularly recorded excitatory junction potentials (e.j.ps) were used as a measure of ATP release and continuous amperometry was used to measure NA release. 2. Varying the extracellular Ca2+ concentration similarly affected the amplitudes of e.j.ps and NA-induced oxidation currents evoked by trains of ten stimuli at 1 Hz. 3. The N-type Ca2+ blocker, omega-conotoxin GVIA (omega-CTX GVIA, 0.1 microM) reduced the amplitudes of both e.j.ps (evoked by trains of ten stimuli at 1 Hz) and NA-induced oxidation currents (evoked by trains of ten stimuli at 1 Hz and 50 stimuli at 10 Hz) by about 90%. 4. The omega-CTX GVIA resistant e.j.ps and NA-induced oxidation currents evoked by trains of 50 stimuli at 10 Hz were abolished by the non-selective Ca2+ channel blocker, Cd2+ (0.1 mM), and were reduced by omega-conotoxin MVIIC (0.5 microM) and omega-agatoxin IVA (40 nM). 5. Nifedipine (10 microm) had no inhibitory effect on omega-CTX GVIA resistant e.j.ps and NA-induced oxidation currents. 6. Thus both varying Ca2+ concentration and applying Ca2+ channel blockers results in similar effects on NA and ATP release from postganglionic sympathetic nerves. These findings are consistent with the hypothesis that NA and ATP are co-released together from the sympathetic nerve terminals.  (+info)

Continuing postischemic neuronal death in CA1: influence of ischemia duration and cytoprotective doses of NBQX and SNX-111 in rats. (2/206)

BACKGROUND AND PURPOSE: Transient forebrain ischemia results in a 24- to 72-hour delayed loss of CA1 neurons. Previous work has not assessed whether insult durations can vary the degree and maturation rate of CA1 injury and whether there are different ultrastructural features of death after brief or severe ischemia. We also tested whether known cytoprotective drugs achieve permanent or transient neuroprotection. METHODS: In the first experiment, ischemia was induced for 5, 15, or 30 minutes with the use of the 4-vessel occlusion rat model with 1- to 28-day survival. Others subjected to 5 or 15 minutes of ischemia and allowed to survive for 14 or 7 days, respectively, were examined with electron microscopy. Finally, we determined whether NBQX (30 mg/kg x3 at 0 or 6 hours after ischemia), an AMPA antagonist, and SNX-111 (5 mg/kg at 6 hours after ischemia), an N-type Ca2+ channel antagonist, provided enduring CA1 protection against 10 minutes of ischemia. RESULTS: CA1 damage was not detected at 24 hours. Thirty minutes of ischemia produced 47% and 84% CA1 damage at 2 and 3 days, respectively. A 15-minute occlusion yielded 11%, 74%, and 86% loss at 2, 3, and 7 days, respectively. Five minutes of ischemia produced an even slower progression with 24%, 52%, and 59% loss at 3, 7, and 14 days, respectively. Ultrastructural examination after 5 and 15 minutes of ischemia revealed necrosis with no morphological evidence of apoptosis. Both NBQX (P<0.021) and SNX-111 (P<0.001) significantly reduced CA1 death at 7 days (/=80%) compared with saline treatment ( approximately 79%). CONCLUSIONS: Brief forebrain ischemia results in a slower progression of CA1 loss than more severe insults. Nonetheless, neuronal injury had necrotic, not apoptotic, morphology. NBQX and SNX-111 only postponed CA1 injury.  (+info)

Calcium influx is required for endocytotic membrane retrieval. (3/206)

Cells use endocytotic membrane retrieval to compensate for excess surface membrane after exocytosis. Retrieval is thought to be calcium-dependent, but the source of this calcium is not known. We found that, in sea urchin eggs, endocytotic membrane retrieval required extracellular calcium. Inhibitors of P-type calcium channels-cadmium, omega-conotoxin MVIIC, omega-agatoxin IVA, and omega-agatoxin TK-blocked membrane retrieval; selective inhibitors of N-type and L-type channels did not. Treatment with calcium ionophores overcame agatoxin inhibition in a calcium-dependent manner. Cadmium blocked membrane retrieval when applied during the first 5 minutes after fertilization, the period when the membrane potential is depolarized. We conclude that calcium influx through omega-agatoxin-sensitive channels plays a key role in signaling for endocytotic membrane retrieval.  (+info)

Biophysical and pharmacological diversity of high-voltage-activated calcium currents in layer II neurones of guinea-pig piriform cortex. (4/206)

1. High-voltage-activated calcium currents were studied with the whole-cell, patch-clamp technique in acutely dissociated pyramidal neurones from guinea-pig piriform cortex layer II. Barium ions were used as charge carriers. 2. Barium currents (IBa) displayed a remarkable kinetic diversity in different neurones. The ratio between the current amplitude at the end of the test pulses and the peak amplitude (Re/p) showed two frequency-distribution peaks at approximately 0.4 and 0.8. The index of current activation speed (rise time 10-90 %) directly correlated with the index of current persistence, Re/p. 3. The half-activation potential (V ) of total IBas positively correlated with the Re/p of the corresponding currents. This implied that the high-decay IBas also had a more negative voltage range of activation than the more persistent ones. 4. The L- and N-type channel blockers nifedipine (10 microM) and omega-conotoxin GVIA (omega-CTx GVIA, 0.5-1 microM) additively blocked 20 and 25 % of the total IBa, respectively. The P/Q-type calcium channel blockers omega-agatoxin IVA (100 nM), omega-conotoxin MVIIC (1 microM) and 3.3 funnel toxin (1 microM), had little effect on IBa. 5. The nifedipine- and omega-CTx GVIA-sensitive current had a Re/p > 0.55 and their voltage dependence of activation was of the high-voltage-activated type (V approximately 0 mV). 6. High-, intermediate- and low-decay blocker-resistant currents were observed in different neurones. Their Re/p values highly correlated with those of the corresponding total IBas and with the voltage dependence of activation of the underlying conductances. Exponential fittings of the inactivation phase of blocker-resistant currents returned very fast time constants (lower than 30 ms) for high-decay currents (Re/p < 0.25). The intermediate-decay currents (Re/p approximately 0.55) could not derive from variable combinations of high- and low-decay current components. 7. Our data demonstrate a remarkable variety in voltage-activated calcium currents expressed by piriform cortex neurones, that include currents resistant to high-voltage-activated calcium-channel blockers.  (+info)

The neuroprotective effects of intrathecal administration of the selective N-type calcium channel blocker ziconotide in a rat model of spinal ischemia. (5/206)

PURPOSE: Spinal cord ischemia and resulting paraplegia represent a major complication associated with surgical repair of the thoracoabdominal aorta. Although the mechanism of spinal neuronal degeneration during ischemia is unclear, it may involve excessive calcium influx via N-type voltage-sensitive calcium channels (VSCCs). The neuroprotective capacity of intrathecal (IT) administration of the selective N-type VSCC blocker ziconotide, previously shown to be potently analgesic, was studied. METHODS: In a rat aortic occlusion model, spinal cord ischemia was induced for 8, 9, or 10 minutes by occluding the descending thoracic aorta. Ziconotide was administered IT as (1) a continuous infusion of 300 or 600 ng/kg/h initiated 24 hours before ischemia and continuing an additional 24 hours or (2) a 0.3 microgram bolus injected 45 minutes before the induction of ischemia. Animals were allowed to live for 24 hours, and recovery of motor function was evaluated during this period. Spinal cords were processed using a silver impregnation technique and microtubule-associated protein type II (MAP2) immunohistochemistry. RESULTS: Continuous IT infusion of ziconotide provided significant protection against 8- and 9-minute occlusions, but not 10-minute occlusions, as indicated by recovery of motor function, degree of spinal neuronal degeneration, and loss of MAP2 immunoreactivity. Acute IT pretreatment with ziconotide provided transient protection during the initial 4 hours of reperfusion; however, this protective effect was no longer present at 24 hours. CONCLUSION: These data implicate N-type VSCC activation in spinal neuronal degeneration caused by transient spinal ischemia, because selective blockade of this channel by continuous IT infusion of ziconotide was protective against injurious intervals of spinal ischemia. Based on these findings, ziconotide may provide both neuroprotection and preemptive analgesia for aortic aneurysm surgery.  (+info)

Differential blockade of rat alpha3beta4 and alpha7 neuronal nicotinic receptors by omega-conotoxin MVIIC, omega-conotoxin GVIA and diltiazem. (6/206)

Rat alpha3beta4 or alpha7 neuronal nicotinic acetylcholine receptors (AChRs) were expressed in Xenopus laevis oocytes, and the effects of various toxins and non-toxin Ca2+ channel blockers studied. Nicotinic AChR currents were elicited by 1 s pulses of dimethylphenylpiperazinium (DMPP, 100 microM) applied at regular intervals. The N/P/Q-type Ca2+ channel blocker omega-conotoxin MVIIC inhibited alpha3beta4 currents with an IC50 of 1.3 microM; the blockade was non-competitive and reversible. The alpha7 currents were unaffected. At 1 microM, omega-conotoxin GVIA (N-type Ca2+ channel blocker) inhibited by 24 and 20% alpha3beta4 and alpha7 currents, respectively. At 1 microM, omega-agatoxin IVA (a P/Q-type Ca2+ channel blocker) did not affect alpha7 currents and inhibited alpha3beta4 currents by only 15%. L-type Ca2+ channel blockers furnidipine, verapamil and, particularly, diltiazem exhibited a preferential blocking activity on alpha3beta4 nicotinic AChRs. The mechanism of alpha3beta4 currents blockade by omega-conotoxins and diltiazem differed in the following aspects: (i) the onset and reversal of the blockade was faster for toxins; (ii) the blockade by the peptides was voltage-dependent, while that exerted by diltiazem was not; (iii) diltiazem promoted the inactivation of the current while omega-toxins did not. These data show that, at concentrations currently employed as Ca2+ channel blockers, some of these compounds also inhibit certain subtypes of nicotinic AChR currents. Our data calls for caution when interpreting many of the results obtained in neurons and other cell types, where nicotinic receptor and Ca2+ channels coexist.  (+info)

Acid-evoked quantal catecholamine secretion from rat phaeochromocytoma cells and its interaction with hypoxia-evoked secretion. (7/206)

1. Amperometric recordings using polarized carbon fibre microelectrodes were used to detect exocytosis of catecholamines from rat phaeochromocytoma (PC12) cells in response to a reduction in pHo. 2. Exocytosis was detected at pHo levels of between 7.2 and 6.8. This was probably due to intracellular acidification, since acid-evoked secretion was enhanced by the Na+-H+ exchange blocker ethylisopropylamiloride (30 microM), and was mimicked by sodium propionate (10 mM), which causes selective intracellular acidosis. 3. Acid-evoked exocytosis was abolished by removal of Ca2+o or application of 200 microM Cd2+. It was unaffected by nifedipine, but significantly reduced by either omega-conotoxin GVIA (1 microM) or omega-agatoxin GIVA (200 nM). The two toxins applied together almost completely abolished (> 97 %) acid-evoked secretion. 4. Hypoxia-evoked catecholamine release was potentiated under acidic conditions and suppressed under alkaline conditions in a manner which indicated a greater than additive interaction of these two stimuli. 5. Our results indicate that, like carotid body arterial chemoreceptors, PC12 cells represent model chemoreceptor cells for both hypoxia and acidity and that the release of catecholamines in response to these physiological stimuli is dependent on Ca2+ influx through voltage-gated N- and P/Q-type Ca2+ channels.  (+info)

delta opioid receptor modulation of several voltage-dependent Ca(2+) currents in rat sensory neurons. (8/206)

Endogenous enkephalins and delta opiates affect sensory function and pain sensation by inhibiting synaptic transmission in sensory circuits via delta opioid receptors (DORs). DORs have long been suspected of mediating these effects by modulating voltage-dependent Ca(2+) entry in primary sensory neurons. However, not only has this hypothesis never been validated in these cells, but in fact several previous studies have only turned up negative results. By using whole-cell current recordings, we show that the delta enkephalin analog [D-Ala(2), D-Leu(5)]-enkephalin (DADLE) inhibits, via DORs, L-, N-, P-, and Q-high voltage-activated Ca(2+) channel currents in cultured rat dorsal root ganglion (DRG) neurons. The percentage of responding cells was remarkably high (75%) within a novel subpopulation of substance P-containing neurons compared with the other cells (18-35%). DADLE (1 microM) inhibited 32% of the total barium current through calcium channels (I(Ba)). A delta (naltrindole, 1 microM), but not a mu (beta-funaltrexamine, 5 microM), antagonist prevented the DADLE response, whereas a DOR-2 subtype (deltorphin-II, 100 nM), but not a DOR-1 (DPDPE, 1 microM), agonist mimicked the response. L-, N-, P-, and Q-type currents contributed, on average, 18, 48, 14, and 16% to the total I(Ba) and 19, 50, 26, and 20% to the DADLE-sensitive current, respectively. The drug-insensitive R-type current component was not affected by the agonist. This work represents the first demonstration that DORs modulate Ca(2+) entry in sensory neurons and suggests that delta opioids could affect diverse Ca(2+)-dependent processes linked to Ca(2+) influx through different high-voltage-activated channel types.  (+info)

Conotoxins are a group of peptide toxins found in the venom of cone snails (genus Conus). These toxins are synthesized and stored in the venom ducts of the snails and are used for prey capture or defense against predators. Conotoxins have diverse pharmacological activities, acting on various ion channels and receptors in the nervous system. They are characterized by their small size (10-30 amino acids), disulfide bonding pattern, and high sequence variability. Due to their specificity and potency, conotoxins have been studied as potential leads for the development of novel therapeutics, particularly in the areas of pain management and neurological disorders.

A Conus snail, also known as a cone snail, is a type of predatory sea snail that belongs to the family Conidae. These snails are known for their venomous harpoons, which they use to capture and immobilize prey. The venom of some species can be dangerous or even deadly to humans.

Conus snails are found in tropical and subtropical waters around the world, and there are over 700 different species. They vary in size, with some species measuring just a few millimeters long and others reaching lengths of several inches. Many Conus snails have brightly colored shells that are highly prized by collectors.

In addition to their medical significance as a source of venom, Conus snails are also of interest to researchers because they produce a variety of bioactive compounds that have potential applications in medicine. For example, some cone snail venoms contain peptides that have been shown to have pain-relieving and neuroprotective properties.

Mollusk venoms are toxic substances produced by certain species of mollusks, a group of marine animals that includes snails, slugs, clams, octopuses, and squids. These venoms are primarily used for defense against predators or for hunting prey. They can contain a variety of bioactive molecules, such as proteins, peptides, and neurotoxins, which can cause a range of effects on the victim's body, from mild irritation to paralysis and death.

One well-known example of a mollusk venom is that of the cone snail, which uses its venom to capture prey. The venom of some cone snails contains compounds called conotoxins, which are highly selective for specific ion channels in the nervous system and can cause paralysis or death in their victims. These conotoxins have been studied for their potential therapeutic applications, such as pain relief and treatment for neurological disorders.

It's important to note that while some mollusk venoms can be dangerous or even deadly to humans, most species of mollusks are not harmful to people. However, it's always a good idea to exercise caution when handling any marine animals, as even non-venomous species can cause injury with their sharp shells or other structures.

I'm sorry for any confusion, but the term "snails" is not a medical term. It is a common name used to refer to a large group of land and sea-dwelling mollusks that have coiled shells and move slowly by means of a muscular foot. If you have any questions about medical terminology or health-related topics, I'd be happy to help! Just let me know what you're looking for.

Nicotinic antagonists are a class of drugs that block the action of nicotine at nicotinic acetylcholine receptors (nAChRs). These receptors are found in the nervous system and are activated by the neurotransmitter acetylcholine, as well as by nicotine. When nicotine binds to these receptors, it can cause the release of various neurotransmitters, including dopamine, which can lead to rewarding effects and addiction.

Nicotinic antagonists work by binding to nAChRs and preventing nicotine from activating them. This can help to reduce the rewarding effects of nicotine and may be useful in treating nicotine addiction. Examples of nicotinic antagonists include mecamylamine, varenicline, and cytisine.

It's important to note that while nicotinic antagonists can help with nicotine addiction, they can also have side effects, such as nausea, vomiting, and abnormal dreams. Additionally, some people may experience more serious side effects, such as seizures or cardiovascular problems, so it's important to use these medications under the close supervision of a healthcare provider.

Disulfides are a type of organic compound that contains a sulfur-sulfur bond. In the context of biochemistry and medicine, disulfide bonds are often found in proteins, where they play a crucial role in maintaining their three-dimensional structure and function. These bonds form when two sulfhydryl groups (-SH) on cysteine residues within a protein molecule react with each other, releasing a molecule of water and creating a disulfide bond (-S-S-) between the two cysteines. Disulfide bonds can be reduced back to sulfhydryl groups by various reducing agents, which is an important process in many biological reactions. The formation and reduction of disulfide bonds are critical for the proper folding, stability, and activity of many proteins, including those involved in various physiological processes and diseases.

Cystine is a naturally occurring amino acid in the body, which is formed from the oxidation of two cysteine molecules. It is a non-essential amino acid, meaning that it can be produced by the body and does not need to be obtained through diet. Cystine plays important roles in various biological processes, including protein structure and antioxidant defense. However, when cystine accumulates in large amounts, it can form crystals or stones, leading to conditions such as cystinuria, a genetic disorder characterized by the formation of cystine kidney stones.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Neurotoxins are substances that are poisonous or destructive to nerve cells (neurons) and the nervous system. They can cause damage by destroying neurons, disrupting communication between neurons, or interfering with the normal functioning of the nervous system. Neurotoxins can be produced naturally by certain organisms, such as bacteria, plants, and animals, or they can be synthetic compounds created in a laboratory. Examples of neurotoxins include botulinum toxin (found in botulism), tetrodotoxin (found in pufferfish), and heavy metals like lead and mercury. Neurotoxic effects can range from mild symptoms such as headaches, muscle weakness, and tremors, to more severe symptoms such as paralysis, seizures, and cognitive impairment. Long-term exposure to neurotoxins can lead to chronic neurological conditions and other health problems.

Sodium channel blockers are a class of medications that work by blocking sodium channels in the heart, which prevents the rapid influx of sodium ions into the cells during depolarization. This action slows down the rate of impulse generation and propagation in the heart, which in turn decreases the heart rate and prolongs the refractory period.

Sodium channel blockers are primarily used to treat cardiac arrhythmias, including atrial fibrillation, atrial flutter, and ventricular tachycardia. They may also be used to treat certain types of neuropathic pain. Examples of sodium channel blockers include Class I antiarrhythmics such as flecainide, propafenone, lidocaine, and mexiletine.

It's important to note that sodium channel blockers can have potential side effects, including proarrhythmia (i.e., the development of new arrhythmias or worsening of existing ones), negative inotropy (decreased contractility of the heart muscle), and cardiac conduction abnormalities. Therefore, these medications should be used with caution and under the close supervision of a healthcare provider.

Nicotinic receptors are a type of ligand-gated ion channel receptor that are activated by the neurotransmitter acetylcholine and the alkaloid nicotine. They are widely distributed throughout the nervous system and play important roles in various physiological processes, including neuronal excitability, neurotransmitter release, and cognitive functions such as learning and memory. Nicotinic receptors are composed of five subunits that form a ion channel pore, which opens to allow the flow of cations (positively charged ions) when the receptor is activated by acetylcholine or nicotine. There are several subtypes of nicotinic receptors, which differ in their subunit composition and functional properties. These receptors have been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, and schizophrenia.

Peptides are short chains of amino acid residues linked by covalent bonds, known as peptide bonds. They are formed when two or more amino acids are joined together through a condensation reaction, which results in the elimination of a water molecule and the formation of an amide bond between the carboxyl group of one amino acid and the amino group of another.

Peptides can vary in length from two to about fifty amino acids, and they are often classified based on their size. For example, dipeptides contain two amino acids, tripeptides contain three, and so on. Oligopeptides typically contain up to ten amino acids, while polypeptides can contain dozens or even hundreds of amino acids.

Peptides play many important roles in the body, including serving as hormones, neurotransmitters, enzymes, and antibiotics. They are also used in medical research and therapeutic applications, such as drug delivery and tissue engineering.

Protein folding is the process by which a protein molecule naturally folds into its three-dimensional structure, following the synthesis of its amino acid chain. This complex process is determined by the sequence and properties of the amino acids, as well as various environmental factors such as temperature, pH, and the presence of molecular chaperones. The final folded conformation of a protein is crucial for its proper function, as it enables the formation of specific interactions between different parts of the molecule, which in turn define its biological activity. Protein misfolding can lead to various diseases, including neurodegenerative disorders such as Alzheimer's and Parkinson's disease.

"Xenopus" is not a medical term, but it is a genus of highly invasive aquatic frogs native to sub-Saharan Africa. They are often used in scientific research, particularly in developmental biology and genetics. The most commonly studied species is Xenopus laevis, also known as the African clawed frog.

In a medical context, Xenopus might be mentioned when discussing their use in research or as a model organism to study various biological processes or diseases.

In genetics, sequence alignment is the process of arranging two or more DNA, RNA, or protein sequences to identify regions of similarity or homology between them. This is often done using computational methods to compare the nucleotide or amino acid sequences and identify matching patterns, which can provide insight into evolutionary relationships, functional domains, or potential genetic disorders. The alignment process typically involves adjusting gaps and mismatches in the sequences to maximize the similarity between them, resulting in an aligned sequence that can be visually represented and analyzed.

High-performance liquid chromatography (HPLC) is a type of chromatography that separates and analyzes compounds based on their interactions with a stationary phase and a mobile phase under high pressure. The mobile phase, which can be a gas or liquid, carries the sample mixture through a column containing the stationary phase.

In HPLC, the mobile phase is a liquid, and it is pumped through the column at high pressures (up to several hundred atmospheres) to achieve faster separation times and better resolution than other types of liquid chromatography. The stationary phase can be a solid or a liquid supported on a solid, and it interacts differently with each component in the sample mixture, causing them to separate as they travel through the column.

HPLC is widely used in analytical chemistry, pharmaceuticals, biotechnology, and other fields to separate, identify, and quantify compounds present in complex mixtures. It can be used to analyze a wide range of substances, including drugs, hormones, vitamins, pigments, flavors, and pollutants. HPLC is also used in the preparation of pure samples for further study or use.

The cysteine arrangements are the same for omega, delta and kappa families, even though omega conotoxins are calcium channel ... Omega, delta and kappa families of conotoxins have a knottin or inhibitor cystine knot scaffold. The knottin scaffold is a very ... Nielsen KJ, Schroeder T, Lewis R (2000). "Structure-activity relationships of omega-conotoxins at N-type voltage-sensitive ... Mu-conotoxins have two types of cysteine arrangements, but the knottin scaffold is not observed. Mu-conotoxins target the ...
"The alpha2delta auxiliary subunit reduces affinity of omega-conotoxins for recombinant N-type (Cav2.2) calcium channels". The ...
They are relatively homologous to the calcium channel blockers omega-conotoxins from marine cone snails and belong to the four- ...
... conotoxins MeSH D20.888.590.162.720 - omega-conotoxins MeSH D20.888.590.162.720.700 - omega-conotoxin gvia MeSH D20.888.590.325 ... omega-agatoxin iva MeSH D20.888.065.970 - wasp venoms MeSH D20.888.230 - cnidarian venoms MeSH D20.888.370 - fish venoms MeSH ...
... conotoxins MeSH D23.946.580.590.162.720 - omega-conotoxins MeSH D23.946.580.590.162.720.700 - omega-conotoxin gvia MeSH D23.946 ... conotoxins MeSH D23.946.833.590.162.720 - omega-conotoxins MeSH D23.946.833.590.162.720.700 - omega-conotoxin gvia MeSH D23.946 ... omega-agatoxin iva MeSH D23.946.833.065.970 - wasp venoms MeSH D23.946.833.230 - cnidarian venoms MeSH D23.946.833.370 - fish ...
Conotoxins represent a category of poisons produced by the marine cone snail, and are capable of inhibiting the activity of a ... McCleskey, E. W. (1987). "Omega-conotoxin: Direct and Persistent Blockade of Specific Types of Calcium Channels in Neurons but ... One of the unique forms of conotoxins, ω-conotoxin (ω-CgTx) is highly specific for Ca channels and has shown usefulness in ... In many cases, the toxins released by the different types of cone snails include a range of different types of conotoxins, ...
ω-Conotoxins are derived from the venom of cone snails. ω-Conotoxin MVIIC acts within the hippocampal CA1 pyramidal neurons to ... omega-agatoxin TK, was used to block the channel. When blocked, patients no longer benefited from the anti-epileptic effects ...
The cysteine arrangements are the same for omega, delta and kappa families, even though omega conotoxins are calcium channel ... Omega, delta and kappa families of conotoxins have a knottin or inhibitor cystine knot scaffold. The knottin scaffold is a very ... Nielsen KJ, Schroeder T, Lewis R (2000). "Structure-activity relationships of omega-conotoxins at N-type voltage-sensitive ... Mu-conotoxins have two types of cysteine arrangements, but the knottin scaffold is not observed. Mu-conotoxins target the ...
Superfamily j.30.1: Conotoxins [58465] (7 families) all apart omega class; it is not a true superfamily. ... Fold j.30: Conotoxins [58464] (1 superfamily). disulfide-rich fold. *. ...
2013) Spinal actions of omega-conotoxins, CVID, MVIIA and related peptides in a rat neuropathic pain model. Br J Pharmacol 170: ...
omega-Conotoxins. 1. 1995. 3. 0.140. Why? Genotyping Techniques. 1. 2015. 79 ...
OMEGA-CONOTOXINAS. OMEGA-CONOTOXINS. ÔMEGA-CONOTOXINAS. ORGANIZADORES EMBRIONARIOS. ORGANIZERS, EMBRYONIC. ORGANIZADORES ... OMEGA-AGATOXINA IVA. OMEGA-AGATOXIN IVA. ÔMEGA-AGATOXINA IVA. OMEGA-CONOTOXINA GVIA. OMEGA-CONOTOXIN GVIA. ÔMEGA-CONOTOXINA ...
OMEGA-CONOTOXINAS. OMEGA-CONOTOXINS. ÔMEGA-CONOTOXINAS. ORGANIZADORES EMBRIONARIOS. ORGANIZERS, EMBRYONIC. ORGANIZADORES ... OMEGA-AGATOXINA IVA. OMEGA-AGATOXIN IVA. ÔMEGA-AGATOXINA IVA. OMEGA-CONOTOXINA GVIA. OMEGA-CONOTOXIN GVIA. ÔMEGA-CONOTOXINA ...
OMEGA-CONOTOXINAS. OMEGA-CONOTOXINS. ÔMEGA-CONOTOXINAS. ORGANIZADORES EMBRIONARIOS. ORGANIZERS, EMBRYONIC. ORGANIZADORES ... OMEGA-AGATOXINA IVA. OMEGA-AGATOXIN IVA. ÔMEGA-AGATOXINA IVA. OMEGA-CONOTOXINA GVIA. OMEGA-CONOTOXIN GVIA. ÔMEGA-CONOTOXINA ...
OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ÔMEGA-CONOTOXINAS ONCOGENE PROTEINS V-MYB PROTEINAS ONCOGENICAS V-MYB PROTEÍNAS ONCOGÊNICAS ... OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINA GVIA ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-AGATOXINA IVA ...
OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ÔMEGA-CONOTOXINAS ONCOGENE PROTEINS V-MYB PROTEINAS ONCOGENICAS V-MYB PROTEÍNAS ONCOGÊNICAS ... OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINA GVIA ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-AGATOXINA IVA ...
OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINAS OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-CONOTOXINA GVIA ...
OMEGA-CONOTOXINAS. OMEGA-CONOTOXINS. ÔMEGA-CONOTOXINAS. ORGANIZADORES EMBRIONARIOS. ORGANIZERS, EMBRYONIC. ORGANIZADORES ... OMEGA-AGATOXINA IVA. OMEGA-AGATOXIN IVA. ÔMEGA-AGATOXINA IVA. OMEGA-CONOTOXINA GVIA. OMEGA-CONOTOXIN GVIA. ÔMEGA-CONOTOXINA ...
OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ÔMEGA-CONOTOXINAS ONCOGENE PROTEINS V-MYB PROTEINAS ONCOGENICAS V-MYB PROTEÍNAS ONCOGÊNICAS ... OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINA GVIA ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-AGATOXINA IVA ...
OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINAS OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-CONOTOXINA GVIA ...
OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ÔMEGA-CONOTOXINAS ONCOGENE PROTEINS V-MYB PROTEINAS ONCOGENICAS V-MYB PROTEÍNAS ONCOGÊNICAS ... OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINA GVIA ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-AGATOXINA IVA ...
OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ÔMEGA-CONOTOXINAS ONCOGENE PROTEINS V-MYB PROTEINAS ONCOGENICAS V-MYB PROTEÍNAS ONCOGÊNICAS ... OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINA GVIA ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-AGATOXINA IVA ...
OMEGA-CONOTOXIN GVIA OMEGA-CONOTOXINA GVIA ÔMEGA-CONOTOXINAS OMEGA-CONOTOXINS OMEGA-CONOTOXINAS ... OMEGA-AGATOXIN IVA OMEGA-AGATOXINA IVA ÔMEGA-CONOTOXINA GVIA ...
Novel omega-conotoxins from Conus catus discriminate among neuronal calcium channel subtypes. Journal of Biological Chemistry, ... Davis, J, Jones, Al and Lewis, R. J. (2009). Remarkable inter- and intra-species complexity of conotoxins revealed by LC/MS. ... Chemical and functional identification and characterization of novel sulfated alpha-conotoxins from the cone snail Conus ...
Calcium channel blockers such as conotoxins have shown a great potential to reduce brain and spinal cord injury. MVIIC ... the omega-conotoxins and omega-agatoxins. Annu Rev Biochem 1994, 63: 823-867. 10.1146/annurev.bi.63.070194.004135 ... including the conotoxins from Conus snails [12]. Omega-conotoxin MVIIC (MVIIC) is a member of the CCB toxin family constituted ... Calcium channel blockers such as conotoxins have shown a great potential to reduce brain and spinal cord injury. MVIIC ...
Constrained de novo sequencing of conotoxins. J Proteome Res. 2012;11(8):4191-200.. Karbat I, Turkov M, Cohen L, et al. X-ray ... Neuronal calcium-channel antagonistsdiscrimination between calcium-channel subtypes using omega-conotoxin from Conus magus ... Genes expressed in a turrid venom duct: divergence and similarity to conotoxins. J Mol Evol. 2006;62(3):247-56.. The Cone Snail ...
Kits,K.S., Lodder,J.C., van der Schors,R.C., Li,K.W., Geraerts,W.P. and Fainzilber,M. (1996) Novel omega-conotoxins block ... the database of conotoxins (http://www.conoserver.org) and the above reference is cited. For any other use please contact David ...
Omega-Conotoxins, Animals, Rats. ...
µ-Conotoxins are small, potent, peptide voltage-gated sodium (NaV) channel inhibitors characterised by a conserved cysteine ... ACS Omega ; 8(29): 26276-26286, 2023 Jul 25. Artigo em Inglês , MEDLINE , ID: mdl-37521635 ... Analysis of other µ-conotoxins at hNaV1.7 shows that only a limited number are capable of inhibition at this subtype and that ... Here, we evaluated and compared the inhibitory potency of µ-conotoxins SxIIIC, SmIIIA and KIIIA at hNaV channels by whole-cell ...
... by comparison with omega-Conotoxin-MVIIA (omega-CTX-MVIIA) and morphine hydrochloride in the formalin test in conscious rats. ... huwena venom similar to micro O-conotoxins MrVIA and MrVIB. ... Similar to omega-CTX-MVIIA and morphine, intrathecal pre- ... than that of HWTX-I and omega-CTX-MVIIA (about 4- 5 h at 1.0 microg/kg). Therefore, the present results show that, like omega- ... the antinociceptive effect of HWTX-I was identical to that of omega-CTX-MVIIA, while omega-CTX-MVIIA acted more remarkably than ...
... the database of conotoxins (http://www.conoserver.org) and the above reference is cited. For any other use please contact David ... omega conotoxin Sequence. CKRKGSSCRRTMYDCCTGSCRNGKC(nh2) ...
omega-Conotoxin GVIA omega-Conotoxins omega-Crystallins omega-N-Methylarginine Omenn Syndrome use Severe Combined ... Omega-3 Fatty Acids use Fatty Acids, Omega-3 Omega-6 Fatty Acids use Fatty Acids, Omega-6 ...
ACS Omega. 8, 22, p. 20085-20095 11 p.. Research output: Contribution to journal › Article › peer-review ...
S-conotoxins - Inhibit 5-HT3 channels Y-conotoxins - Competitively block muscle acetylcholine receptors ... Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American ... Venom, with different conotoxins formed rapidly in various portions of the venom duct due to different conotoxin gene ... Several conotoxins, and their synthetic derivatives, due to their high selectivity and affinity for different ion channels, are ...
Nutraceuticals listed on FLCCC Protocols, including Vitamin C, Vitamin D with K2, Omega-3 fatty acids, Nigella Sativa, N-Acetyl ... More information on snake venom and conotoxins, spike proteins and the covid 19 vaccines ...
Omega-conopeptide-mediated maximum inhibition of norepinephrine release from tail arteries ranged from 11.2% to 36.9% of ... The interaction of ω-conotoxins with non-L-type VSCCs in brain synaptosomal preparations has been investigated with the aid of ... References Abe T, Koyano K, Saisu H, Nishiuchi Y, Sakakibara S (1986) Binding of omega-conotoxin to receptor sites associated ... Neuropharmacology 32: 1075-1088 Zhao Q, Smith M-L, Siesjö BK (1994) The omega-conopeptide, SNX-111, an N-type calcium channel ...
  • A wide variety of natural CCB were identified in animal venoms containing neuroactive or neuroprotective peptides, including the conotoxins from Conus snails [ 12 ]. (biomedcentral.com)
  • Conotoxins, which are peptides consisting of 10 to 30 amino acid residues, typically have one or more disulfide bonds. (wikipedia.org)
  • The cysteine arrangements are the same for omega, delta and kappa families, even though omega conotoxins are calcium channel blockers, whereas delta conotoxins delay the inactivation of sodium channels, and kappa conotoxins are potassium channel blockers. (wikipedia.org)
  • Calcium channel blockers such as conotoxins have shown a great potential to reduce brain and spinal cord injury. (biomedcentral.com)
  • Each of the five types of conotoxins attacks a different target: α-conotoxin inhibits nicotinic acetylcholine receptors at nerves and muscles. (wikipedia.org)
  • Over the last few decades conotoxins have been the subject of pharmacological interest. (wikipedia.org)
  • The disulfide bonding network, as well as specific amino acids in inter-cysteine loops, provide the specificity of conotoxins. (wikipedia.org)
  • Alpha conotoxins have two types of cysteine arrangements, and are competitive nicotinic acetylcholine receptor antagonists. (wikipedia.org)
  • Mu-conotoxins have two types of cysteine arrangements, but the knottin scaffold is not observed. (wikipedia.org)
  • Omega, delta and kappa families of conotoxins have a knottin or inhibitor cystine knot scaffold. (wikipedia.org)
  • In this study, we sought to combine the pore blocking activity of conotoxins with the gating modifier activity of spider toxins to design new bivalent inhibitors of NaV1.7 with improved potency and selectivity. (bvsalud.org)
  • Conotoxins, which are peptides consisting of 10 to 30 amino acid residues, typically have one or more disulfide bonds. (wikipedia.org)
  • Omega, delta and kappa families of conotoxins have a knottin or inhibitor cystine knot scaffold. (wikipedia.org)
  • The cysteine arrangements are the same for omega, delta and kappa families, even though omega conotoxins are calcium channel blockers, whereas delta conotoxins delay the inactivation of sodium channels, and kappa conotoxins are potassium channel blockers. (wikipedia.org)
  • Conotoxins have a variety of mechanisms of actions, most of which have not been determined. (wikipedia.org)
  • Omega toxins inhibit the actions of these channels by altering their voltage dependence. (lookformedical.com)
  • Mu-conotoxins target the muscle-specific voltage-gated sodium channels, and are useful probes for investigating voltage-dependent sodium channels of excitable tissues. (wikipedia.org)
  • Different subtypes of voltage-gated sodium channels are found in different tissues in mammals, e.g., in muscle and brain, and studies have been carried out to determine the sensitivity and specificity of the mu-conotoxins for the different isoforms. (wikipedia.org)