Neurotoxic proteins from the venom of the banded or Formosan krait (Bungarus multicinctus, an elapid snake). alpha-Bungarotoxin blocks nicotinic acetylcholine receptors and has been used to isolate and study them; beta- and gamma-bungarotoxins act presynaptically causing acetylcholine release and depletion. Both alpha and beta forms have been characterized, the alpha being similar to the large, long or Type II neurotoxins from other elapid venoms.
Surgical reinnervation of a denervated peripheral target using a healthy donor nerve and/or its proximal stump. The direct connection is usually made to a healthy postlesional distal portion of a non-functioning nerve or implanted directly into denervated muscle or insensitive skin. Nerve sprouts will grow from the transferred nerve into the denervated elements and establish contact between them and the neurons that formerly controlled another area.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Venoms from snakes of the family Elapidae, including cobras, kraits, mambas, coral, tiger, and Australian snakes. The venoms contain polypeptide toxins of various kinds, cytolytic, hemolytic, and neurotoxic factors, but fewer enzymes than viper or crotalid venoms. Many of the toxins have been characterized.
A specific complex of toxic proteins from the venom of Crotalus durissus terrificus (South American rattlesnake). It can be separated into a phospholipase A and crotapotin fragment; the latter consists of three different amino acid chains, potentiates the enzyme, and is specifically neurotoxic.
A genus of poisonous snakes of the subfamily Elapinae of the family ELAPIDAE. They comprise the kraits. Twelve species are recognized and all inhabit southeast Asia. They are considered extremely dangerous. (Moore: Poisonous Snakes of the World, 1980, p120)
A potent inhibitor of the high affinity uptake system for CHOLINE. It has less effect on the low affinity uptake system. Since choline is one of the components of ACETYLCHOLINE, treatment with hemicholinium can deplete acetylcholine from cholinergic terminals. Hemicholinium 3 is commonly used as a research tool in animal and in vitro experiments.
Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.
A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.
The portion of an interactive computer program that issues messages to and receives commands from a user.
Sequential operating programs and data which instruct the functioning of a digital computer.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
A process that includes the determination of AMINO ACID SEQUENCE of a protein (or peptide, oligopeptide or peptide fragment) and the information analysis of the sequence.
Serum albumin from cows, commonly used in in vitro biological studies. (From Stedman, 25th ed)
Polymers of ETHYLENE OXIDE and water, and their ethers. They vary in consistency from liquid to solid depending on the molecular weight indicated by a number following the name. They are used as SURFACTANTS, dispersing agents, solvents, ointment and suppository bases, vehicles, and tablet excipients. Some specific groups are NONOXYNOLS, OCTOXYNOLS, and POLOXAMERS.
Cells derived from the BLASTOCYST INNER CELL MASS which forms before implantation in the uterine wall. They retain the ability to divide, proliferate and provide progenitor cells that can differentiate into specialized cells.
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.
Widely used technique which exploits the ability of complementary sequences in single-stranded DNAs or RNAs to pair with each other to form a double helix. Hybridization can take place between two complimentary DNA sequences, between a single-stranded DNA and a complementary RNA, or between two RNA sequences. The technique is used to detect and isolate specific sequences, measure homology, or define other characteristics of one or both strands. (Kendrew, Encyclopedia of Molecular Biology, 1994, p503)
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A family of extremely venomous snakes, comprising coral snakes, cobras, mambas, kraits, and sea snakes. They are widely distributed, being found in the southern United States, South America, Africa, southern Asia, Australia, and the Pacific Islands. The elapids include three subfamilies: Elapinae, Hydrophiinae, and Lauticaudinae. Like the viperids, they have venom fangs in the front part of the upper jaw. The mambas of Africa are the most dangerous of all snakes by virtue of their size, speed, and highly toxic venom. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p329-33)
A selective nicotinic cholinergic agonist used as a research tool. DMPP activates nicotinic receptors in autonomic ganglia but has little effect at the neuromuscular junction.
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.
Sensory cells of organ of Corti. In mammals, they are usually arranged in three or four rows, and away from the core of spongy bone (the modiolus), lateral to the INNER AUDITORY HAIR CELLS and other supporting structures. Their cell bodies and STEREOCILIA increase in length from the cochlear base toward the apex and laterally across the rows, allowing differential responses to various frequencies of sound.
An alkaloid found in the seeds of STRYCHNOS NUX-VOMICA. It is a competitive antagonist at glycine receptors and thus a convulsant. It has been used as an analeptic, in the treatment of nonketotic hyperglycinemia and sleep apnea, and as a rat poison.
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.
Plant extracts from several species, including genera STRYCHNOS and Chondodendron, which contain TETRAHYDROISOQUINOLINES that produce PARALYSIS of skeletal muscle. These extracts are toxic and must be used with the administration of artificial respiration.
Sensory cells in the organ of Corti, characterized by their apical stereocilia (hair-like projections). The inner and outer hair cells, as defined by their proximity to the core of spongy bone (the modiolus), change morphologically along the COCHLEA. Towards the cochlear apex, the length of hair cell bodies and their apical STEREOCILIA increase, allowing differential responses to various frequencies of sound.
The part of the inner ear (LABYRINTH) that is concerned with hearing. It forms the anterior part of the labyrinth, as a snail-like structure that is situated almost horizontally anterior to the VESTIBULAR LABYRINTH.
Auditory sensory cells of organ of Corti, usually placed in one row medially to the core of spongy bone (the modiolus). Inner hair cells are in fewer numbers than the OUTER AUDITORY HAIR CELLS, and their STEREOCILIA are approximately twice as thick as those of the outer hair cells.
A compound that contains a reduced purine ring system but is not biosynthetically related to the purine alkaloids. It is a poison found in certain edible mollusks at certain times; elaborated by GONYAULAX and consumed by mollusks, fishes, etc. without ill effects. It is neurotoxic and causes RESPIRATORY PARALYSIS and other effects in MAMMALS, known as paralytic SHELLFISH poisoning.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
The covalent bonding of an alkyl group to an organic compound. It can occur by a simple addition reaction or by substitution of another functional group.
Chemical agents that react with SH groups. This is a chemically diverse group that is used for a variety of purposes. Among these are enzyme inhibition, enzyme reactivation or protection, and labelling.
A standard reagent for the determination of reactive sulfhydryl groups by absorbance measurements. It is used primarily for the determination of sulfhydryl and disulfide groups in proteins. The color produced is due to the formation of a thio anion, 3-carboxyl-4-nitrothiophenolate.
Analogs of those substrates or compounds which bind naturally at the active sites of proteins, enzymes, antibodies, steroids, or physiological receptors. These analogs form a stable covalent bond at the binding site, thereby acting as inhibitors of the proteins or steroids.
A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.
An opisthobranch mollusk of the order Anaspidea. It is used frequently in studies of nervous system development because of its large identifiable neurons. Aplysiatoxin and its derivatives are not biosynthesized by Aplysia, but acquired by ingestion of Lyngbya (seaweed) species.
A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.
A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Hormones produced by invertebrates, usually insects, mollusks, annelids, and helminths.
Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.
Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.
Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.
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.
A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. It consists entirely of pentameric a7 subunits expressed in the CNS, autonomic nervous system, vascular system, lymphocytes and spleen.
A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.
A C19 norditerpenoid alkaloid (DITERPENES) from the root of ACONITUM plants. It activates VOLTAGE-GATED SODIUM CHANNELS. It has been used to induce ARRHYTHMIAS in experimental animals and it has antiinflammatory and antineuralgic properties.
A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A family of neurotransmitter transporter proteins that are INTEGRAL MEMBRANE PROTEINS of the LIPID BILAYER of SECRETORY VESICLES. They are ANTIPORTERS that exchange vesicular PROTONS for cytoplasmic NEUROTRANSMITTER and play an essential role in regulating neurotransmission.
A very loosely defined group of drugs that tend to reduce the activity of the central nervous system. The major groups included here are ethyl alcohol, anesthetics, hypnotics and sedatives, narcotics, and tranquilizing agents (antipsychotics and antianxiety agents).
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Membrane transport proteins found predominately in NEURONS and neuroendocrine cells that facilitate neurotransmitter transport. They include two distinct families of proteins that transport NEUROTRANSMITTERS across the PLASMA MEMBRANE and that transport NEUROTRANSMITTERS into SECRETORY VESICLES.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.

Nerve terminal damage by beta-bungarotoxin: its clinical significance. (1/911)

We report here original data on the biological basis of prolonged neuromuscular paralysis caused by the toxic phospholipase A2 beta-bungarotoxin. Electron microscopy and immunocytochemical labeling with anti-synaptophysin and anti-neurofilament have been used to show that the early onset of paralysis is associated with the depletion of synaptic vesicles from the motor nerve terminals of skeletal muscle and that this is followed by the destruction of the motor nerve terminal and the degeneration of the cytoskeleton of the intramuscular axons. The postjunctional architecture of the junctions were unaffected and the binding of fluorescein-isothiocyanate-conjugated alpha-bungarotoxin to acetylcholine receptor was not apparently affected by exposure to beta-bungarotoxin. The re-innervation of the muscle fiber was associated by extensive pre- and post-terminal sprouting at 3 to 5 days but was stable by 7 days. Extensive collateral innervation of adjacent muscle fibers was a significant feature of the re-innervated neuromuscular junctions. These findings suggest that the prolonged and severe paralysis seen in victims of envenoming bites by kraits (elapid snakes of the genus Bungarus) and other related snakes of the family Elapidae is caused by the depletion of synaptic vesicles from motor nerve terminals and the degeneration of the motor nerve terminal and intramuscular axons.  (+info)

Selective effects of a 4-oxystilbene derivative on wild and mutant neuronal chick alpha7 nicotinic receptor. (2/911)

1. We assessed the pharmacological activity of triethyl-(beta-4-stilbenoxy-ethyl) ammonium (MG624), a drug that is active on neuronal nicotinic receptors (nicotinic AChR). Experiments on the major nicotinic AChR subtypes present in chick brain, showed that it inhibits the binding of [125I]-alphaBungarotoxin (alphaBgtx) to the alpha7 subtype, and that of [3H]-epibatidine (Epi) to the alpha4beta2 subtype, with Ki values of respectively 106 nM and 84 microM. 2. MG624 also inhibited ACh elicited currents (I(ACh)) in the oocyte-expressed alpha7 and alpha4beta2 chick subtypes with half-inhibitory concentrations (IC50) of respectively 109 nM and 3.2 microM. 3. When tested on muscle-type AChR, it inhibited [125I]-alphaBgtx binding with a Ki of 32 microM and ACh elicited currents (I(ACh)) in the oocyte-expressed alpha1beta1gammadelta chick subtype with an IC50 of 2.9 microM. 4. The interaction of MG624 with the alpha7 subtype was investigated using an alpha7 homomeric mutant receptor with a threonine-for-leucine 247 substitution (L247T alpha7). MG624 did not induce any current in oocytes expressing the wild type alpha7 receptor, but did induce large currents in the oocyte-expressed L247T alpha7 receptor. The MG624 elicited current (I(MG62)) has an EC50 of 0.2 nM and a Hill coefficient nH of 1.9, and is blocked by the nicotinic receptor antagonist methyllycaconitine (MLA). 5. These binding and electrophysiological studies show that MG624 is a potent antagonist of neuronal chick alpha7 nicotinic AChR, and becomes a competitive agonist following the mutation of the highly conserved leucine residue 247 located in the M2 channel domain.  (+info)

Synaptic transmission at nicotinic acetylcholine receptors in rat hippocampal organotypic cultures and slices. (3/911)

1. Whole-cell clamp recordings of the compound synaptic current elicited by afferent stimulation of Schaffer collaterals showed that blockade of the NMDA, AMPA and GABAA receptor-mediated components by 6-nitro-7-sulphamoyl- benzo(f)quinoxaline-2,3-dione (NBQX), 3-((R)-2-carboxypiperazine-4-yl)propyl-1-phosphonate (R-CPP) and picrotoxin, respectively, left a small residual current in 39 out of 41 CA1 pyramidal neurones in organotypic cultures and 9 out of 16 CA1 cells in acutely prepared slices. 2. This current represented 2. 9 +/- 0.4 % of the compound evoked synaptic response in organoypic cultures and 1.4 +/- 0.5 % in slices. It was characterized by a slightly rectifying I-V curve and a reversal potential of 3.4 +/- 5. 1 mV. 3. This residual current was insensitive to blockers of GABAB, purinergic, muscarinic and 5-HT3 receptors, but it was essentially blocked by the nicotinic receptor antagonist d-tubocurarine (91 +/- 4 % blockade; 20 microM), and partly blocked by alpha-bungarotoxin (200 nM) and methyllycaconitine (10 nM), two antagonists with a higher selectivity for alpha7 subunit-containing nicotinic receptors (48 +/- 3 % and 55 +/- 11 % blockade, respectively). 4. The residual current was of synaptic origin, since it occurred after a small delay; its amplitude depended upon the stimulation intensity and it was calcium dependent and blocked by the sodium channel antagonist tetrodotoxin. 5. We conclude that afferent stimulation applied in the stratum radiatum evokes in some hippocampal neurones a small synaptic current mediated by activation of neuronal nicotinic receptors.  (+info)

Local alpha-bungarotoxin-sensitive nicotinic receptors modulate hippocampal norepinephrine release by systemic nicotine. (4/911)

Previous studies have shown that nicotinic receptors (NAChRs) accessible from the cerebral aqueduct of the brainstem mediate the hippocampal norepinephrine (NE) release induced by i.v. nicotine. The present study was designed to investigate the role of hippocampal NAChRs in this process. Nicotinic antagonists were microinjected or microdialyzed into the hippocampus (HP) before administering nicotine (0.09 mg/kg over 60 s, i.v.) to freely moving rats. alpha-Bungarotoxin (0.3 nmol by microinjection) blocked nicotine-induced hippocampal NE release by 47% (p <.05) and abolished the effect of 0.065 mg/kg nicotine. Methyllycaconitine (1.4-5.6 mM in the dialysate) inhibited the stimulatory effect of nicotine 0.09 mg/kg by 48 to 75% (p <.05). In contrast, mecamylamine (2.9-5.8 mM) and dihydro-beta-erythroidine (7-14 mM) were completely ineffective. The role of hippocampal NAChRs was demonstrated further by selectively desensitizing these receptors before the systemic infusion of nicotine. To do so, the HP was pretreated with nicotine (0.1 mM) delivered through the microdialysis probe; this concentration was calculated to yield tissue concentrations similar to those produced by the systemic infusions of nicotine. Dialyzing this concentration of nicotine into the HP inhibited the NE response to i.v. nicotine by 34% (p <.05), and 1.0 mM nicotine reduced the response by 40%. These studies indicate that alpha-bungarotoxin-sensitive hippocampal NAChRs, probably containing alpha7 subunits, modulate hippocampal NE release because of systemic nicotine.  (+info)

Waglerin-1 selectively blocks the epsilon form of the muscle nicotinic acetylcholine receptor. (5/911)

Neonatal mice resist the lethal effect of Waglerin-1. Because Waglerin-1 blocks the nicotinic acetylcholine receptor of mature end-plates, the appearance of lethality may result from the epsilon- for gamma-subunit substitution. In support of this hypothesis, adult knockout (KO) mice lacking the gene coding for the epsilon-subunit resist the lethal effect of Waglerin-1. In contrast, heterozygous litter mates respond to Waglerin-1 like adult wild-type mice. In vitro application of 1 microM Waglerin-1 inhibited spontaneous miniature end-plate potentials and evoked end-plate potentials of adult wild-type and heterozygous KO mice. Both miniature end-plate potentials and end-plate potentials of neonatal wild-type and adult homozygous KO mice resisted Waglerin-1. Waglerin-1 decreased the end-plate response of adult wild-type mice to iontophoretically applied acetylcholine (ACh) with an IC50 value of 50 nM; 1 microM Waglerin-1 decreased the ACh response to 4 +/- 1% of control for adult heterozygous KO mice. In contrast, 1 microM Waglerin-1 decreased the ACh response to 73 +/- 2% of control for wild-type mice less than 11 days old and had no effect on the ACh response of adult homozygous KO mice. Between 11 and 12 days after birth, the suppressant effect of Waglerin-1 on wild-type end-plate responses to ACh dramatically increased. Waglerin-1 reduced binding of alpha-bungarotoxin to end-plates of adult but not neonatal wild-type mice. These data demonstrate that Waglerin-1 selectively blocks the mouse muscle nicotinic acetylcholine receptor containing the epsilon-subunit.  (+info)

Subunit interface selectivity of the alpha-neurotoxins for the nicotinic acetylcholine receptor. (6/911)

Peptide toxins selective for particular subunit interfaces of the nicotinic acetylcholine receptor have proven invaluable in assigning candidate residues located in the two binding sites and for determining probable orientations of the bound peptide. We report here on a short alpha-neurotoxin from Naja mossambica mossambica (NmmI) that, similar to other alpha-neurotoxins, binds with high affinity to alphagamma and alphadelta subunit interfaces (KD approximately 100 pM) but binds with markedly reduced affinity to the alphaepsilon interface (KD approximately 100 nM). By constructing chimeras composed of portions of the gamma and epsilon subunits and coexpressing them with wild type alpha, beta, and delta subunits in HEK 293 cells, we identify a region of the subunit sequence responsible for the difference in affinity. Within this region, gammaPro-175 and gammaGlu-176 confer high affinity, whereas Thr and Ala, found at homologous positions in epsilon, confer low affinity. To identify an interaction between gammaGlu-176 and residues in NmmI, we have examined cationic residues in the central loop of the toxin and measured binding of mutant toxin-receptor combinations. The data show strong pairwise interactions or coupling between gammaGlu-176 and Lys-27 of NmmI and progressively weaker interactions with Arg-33 and Arg-36 in loop II of this three-loop toxin. Thus, loop II of NmmI, and in particular the face of this loop closest to loop III, appears to come into close apposition with Glu-176 of the gamma subunit surface of the binding site interface.  (+info)

The effects of beta-bungarotoxin on the morphogenesis of taste papillae and taste buds in the mouse. (7/911)

Although it has been long accepted that innervation by a taste nerve is essential for maintenance of taste buds, it is not clear what role, if any, innervation plays in the morphogenesis of taste papillae and taste bud development. The following study was undertaken to determine what effects lack of sensory innervation have on the development of taste papillae and the formation of taste buds in the mouse. Timed-pregnant female mice (n = 3) at gestational day 12 (gd12) were anesthetized and a 1 microl solution (1 microg/microl) of beta-bungarotoxin (beta-BTX), a neurotoxin that disrupts sensory and motor neuron development, was injected into the amniotic cavity of two embryos per dam. Two shams were injected with PBS. Fetuses were harvested at gd18, 1 day before birth, and four beta-BTX-injected embryos, two shams and two controls were fixed in buffered paraformaldehyde. Serial sections were examined for the presence and morphology of taste papillae and taste buds. No nerve profiles were observed in beta-BTX-injected tongues. Although circumvallate papillae were present on beta-BTX tongues, only five fungiform papillae could be identified. Taste buds were present on a large percentage of fungiform papillae profiles (24%) and on circumvallate papillae in sham and control fetuses; in contrast, no taste buds were associated with taste papillae in beta-BTX fetuses. These results implicate a significant role for innervation in taste papillae and taste bud morphogenesis.  (+info)

Stress-activated protein kinase-3 interacts with the PDZ domain of alpha1-syntrophin. A mechanism for specific substrate recognition. (8/911)

Mechanisms for selective targeting to unique subcellular sites play an important role in determining the substrate specificities of protein kinases. Here we show that stress-activated protein kinase-3 (SAPK3, also called ERK6 and p38gamma), a member of the mitogen-activated protein kinase family that is abundantly expressed in skeletal muscle, binds through its carboxyl-terminal sequence -KETXL to the PDZ domain of alpha1-syntrophin. SAPK3 phosphorylates alpha1-syntrophin at serine residues 193 and 201 in vitro and phosphorylation is dependent on binding to the PDZ domain of alpha1-syntrophin. In skeletal muscle SAPK3 and alpha1-syntrophin co-localize at the neuromuscular junction, and both proteins can be co-immunoprecipitated from transfected COS cell lysates. Phosphorylation of a PDZ domain-containing protein by an associated protein kinase is a novel mechanism for determining both the localization and the substrate specificity of a protein kinase.  (+info)

TY - JOUR. T1 - Increases in the concentration of brain α-bungarotoxin binding sites induced by dietary choline are age-dependent. AU - Morley, Barbara J.. AU - Garner, Laura L.. PY - 1986/7/23. Y1 - 1986/7/23. N2 - We have previously reported that a diet supplemented with choline induces an increase in the concentration of a brain nicotinic-like receptor, as measured by α-bungarotoxin (BuTX) binding. Here we report the effects of choline administered in the drinking water on BuTX binding in the cortex, midbrain and brainstem of rats at 3 ages. In comparison with animals fed a choline-free diet, choline supplementation produced increases averaging 50% in 23-day-old rats and increases of approximately 30% in 60-day-old rats. Increases were also found in 6-month-old animals (averaging 16%), but the differences were generally not statistically significant. The mechanism responsible for the increase in the concentration of BuTX binding sites following the administration of dietary choline is not ...
Methyllycaconitine (MLA, 1) is a novel, potent probe for mammalian and insect nicotinic acetylcholine receptors (nAChR) and displays remarkable selectivity toward neuronal [125I]-alpha-bungarotoxin (alpha BgTX) binding sites that correspond to alpha 7-type nAChR in mammalian brain. We have shown that, among a number of selected norditerpenoid alkaloids, elatine (2) and nudicauline (3) are equipotent with, or better than, MLA (1) in binding to brain [125I]-alpha BgTX binding sites, with IC50 values of 6.1, 1.7, and 7.6 nM, respectively. The 2-((S)-methylsuccinimido)benzoyl moiety of these ligands is crucial for high-affinity binding, whereas structural modifications to the norditerpenoid core of the ligand can be tolerated without loss of activity or selectivity. In addition to MLA (1), elatine (2), and nudicauline (3), we have examined lycoctonine (4), inuline (6), lappaconitine (7), N-desacetyllappaconitine (8), delsoline (10), delcorine (11), deltaline (12), condelphine (13), and karacoline (14). This
Gentaur molecular products has all kinds of products like :search , Biotium \ alpha_bungarotoxin, CF633 \ 00009 for more molecular products just contact us
Snake venom phospholipase A2 (PLA2) that inhibits neuromuscular transmission by blocking acetylcholine release from the nerve termini. PLA2 catalyzes the calcium-dependent hydrolysis of the 2-acyl groups in 3-sn-phosphoglycerides (By similarity).
The cDNA encoding the A chain ofΒ-bungarotoxin (Β-Bgt) was constructed from the cellular RNA isolated from the venom glands ofBungarus multicinctus (Taiwan banded krait). The deduced amino acid sequen
Cells from a line of transformed quail fibroblasts (QT-6) were transfected with cDNAs coding for subunits of the mouse muscle nicotinic ACh receptor (AChR). Stable clones were selected that expressed subunits of the fetal-type AChR (alpha, beta, gamma, delta) or the adult-type AChR (alpha, beta, epsilon, delta). The receptors had the appropriate burst durations and single-channel conductances for the fetal or adult type, respectively. Each type of receptor had a dose- response relationship that was close to a square law at low concentrations of ACh, implying that they contained two ACh-binding subunits. The metabolic stability of surface fetal and adult receptors was identical (about 10 hr half-life), for two independent clones expressing fetal and two expressing adult AChR. The metabolic stability was unaffected by treatment with okadaic acid, which enhanced receptor phosphorylation. d-Tubocurarine (dTC) blocked both the binding of alpha- bungarotoxin (BTX) to the cells and the ACh-elicited ...
Azanorbornylpurine derivatives were prepared by Mitsunobu reaction of appropriate hydroxyazanorbornane derivative with 6-chloropurine or construction of purine base at azanorbornylamines. The prepared target compounds were evaluated for antiviral activity and effect on neuronal and muscle nicotinic acetylcholine receptors. (C) 2011 Published by Elsevier Ltd ...
Bungarus in Chinese translation, English Chinese dictionary, English Chinese translation, with pronunciation, a lot of example sentences
Atıf İçin Kopyala EDINK E., RUCKTOOA P., RETRA K., Akdemir A. , NAHAR T., ZUIDERVELD O., et al. Journal of the American Chemical Society, cilt.133, ss.5363-71, 2011 (SCI Expanded İndekslerine Giren Dergi) ...
Radiant insights, inc Neuronal Acetylcholine Receptor Subunit Alpha 7 (CHRNA7) - Pipeline Review, H2 2016, provides in depth analysis on Neuronal Acetylcholine Receptor Subunit Alpha 7 (CHRNA7) targeted pipeline therapeutics. The report provides comprehensive information on the Neuronal Acetylcholine Receptor Subunit Alpha 7 (CHRNA7) , targeted therapeutics, complete with analysis by indications, stage of development,…
Elliott, K.J.; Ellis, S.B.; Berckhan, K.J.; Urrutia, A.; Chavez-Noriega, L.E.; Johnson, E.C.; Veliçelebi, G.; Harpold, M.M., 1996: Comparative structure of human neuronal alpha 2-alpha 7 and beta 2-beta 4 nicotinic acetylcholine receptor subunits and functional expression of the alpha 2, alpha 3, alpha 4, alpha 7, beta 2, and beta 4 subunits
Acetylcholine (ACh) is an important neurotransmitter in the mammalian brain; it is implicated in arousal, learning, and other cognitive functions. Recent studies indicate that nicotinic receptors contribute to these cholinergic effects, in addition to the established role of muscarinic receptors. In the hippocampus, where cholinergic involvement in learning and memory is particularly well documented, 7 nicotinic acetylcholine receptor subunits (7 nAChRs) are highly expressed, but their precise ultrastructural localization has not been determined. Here, we describe the results of immunogold labeling of serial ultrathin sections through stratum radiatum of area CA1 in the rat. Using both anti-7 nAChR immunolabeling and -bungarotoxin binding, we find that 7 nAChRs are present at nearly all synapses in CA1 stratum radiatum, with immunolabeling present at both presynaptic and postsynaptic elements. Morphological considerations and double immunolabeling indicate that GABAergic as well as glutamatergic ...
Naturally occurring genetic variability in the nicotinic acetylcholine receptor alpha4 and alpha7 subunit genes and phenotypic diversity in humans and mice Journal Article ...
BioAssay record AID 145983 submitted by ChEMBL: Binding affinity towards rat nicotinic acetylcholine receptor alpha2-beta2 expressed in HEK293 cells using [3H]EB as radioligand.
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Binding of [125I]α-bungarotoxin to acetylcholine receptors of ganglionic homogenate of the marine mollusc Aplysia is blocked by the anticholinesterases eserine (I50 = 4 µM) and neostigmine (I50 = 0.2 mM). The classical acetylcholine antagonist d-tubocurarine blocks with an I50 of 2 µM. Eserine (I50 = 3.2 µM) and neostigmine (I50 , 1 mM) also block toxin binding to a solubilized receptor preparation. In contrast to their relative potency in blocking toxin binding, neostigmine is a more potent inhibitor of Aplysia acetylcholinesterase (I50 = 14 nM) than is eserine (I50 = 250 nM). α-Bungarotoxin does not affect esterase activity or interfere with the ability of eserine to block the esterase. The response to acetylcholine recorded through intracellular microelectrodes is blocked by α-bungarotoxin. Neither eserine nor neostigmine blocks the acetylcholine response; rather, they prolong and increase it, as expected from their effects on the esterase. Eserine (0.1 mM) blocks the α-bungarotoxin ...
Amino acid sequences of three .BETA.-bungarotoxins (.BETA.3-,.BETA.4-, and .BETA.5-bungarotoxins) from Bungarus multicinctus venom. Amino acid substitutions in the A chains. (1982 ...
The norditerpenoid alkaloid methyllycaconitine (MLA) acts as a competitive antagonist on the nicotinic acetylcholine receptor (nAChR) with a high preference for the neuronal α-bungarotoxin (αBgt)-sensitive nAChR over the muscle nAChR in mammals. MLA is thus a useful pharmacological tool. Furthermore, its efficient binding to insect nAChR indicates a high insecticidal potency. Within the complex hexacyclic structure of MLA, we envisaged a potential simple pharmacophore. This led to the design and synthesis of acyclic and monocyclic analogues of MLA. The biological activity of these derivatives at both neuronal nicotinic and muscarinic AChR was evaluated. Some of these structurally simple compounds, despite displaying a modest affinity for the nAChR, showed good specificity. We were able to show the importance of the 2-(methylsuccinimido)benzoate ester moiety and the E-ring of MLA. None of the analogues tested displayed any affinity for [3H]nicotine binding sites in brain membranes, indicating that α7
Two probes previously shown to distinguish the nicotinic ACh receptor of chick ciliary ganglion neurons also recognize a component on the surface of bovine chromaffin cells in culture that displays the properties expected for the chromaffin nicotinic ACh receptor. The first probe is a monoclonal antibody, mAb 35, raised against ACh receptor from Electrophorus electric organ, and the second is an alpha- neurotoxin, Bgt 3.1, purified from B. multicinctus venom. mAb 35 binds specifically to a single class of high-affinity sites on the chromaffin cells in culture. Scatchard analysis indicates a KD of 2.1 +/- 0.2 nM for the binding and a Bmax of 1.6 +/- 0.1 X 10(4) mAb 35 sites per cell. The number of sites on the cells can be reduced through modulation by exposure of the cells to Bgt 3.1. The modulation can be blocked by the cholinergic ligands d-tubocurarine and carbamylcholine. Long-term exposure to the agonist carbamylcholine alone also reduces the number of mAb 35 binding sites. Bgt 3.1 inhibits ...
Our recent study (J Natl Cancer Inst, 102, 1322‐1335, 2010) demonstrated that the α9‐nicotinic receptor (α9‐nAChR) was detected at higher levels in advanced‐stage breast tumor tissues (tumor/normal ,8 fold, n=276) of Taiwanese patients. This research group will focus on α9‐nAChR‐mediated tumorigenesis mechanisms and will establish novel therapeutic strategies to overcome drug resistance in breast cancer. This 3‐year proposal is comprised of the following aims: Year‐1 study: To explore the molecular mechanisms of α9‐nAChR‐mediated carcinogenesis, clinical samples of advanced stage tumor patients will be collected (component project‐1, CP‐1). A molecular epidemiology study of selected family history will be established (CP‐2). The role of breast tumor stem cells in advanced‐stage breast cancer and the development of stem cell‐killing drugs will be explored (CP‐3). Validation of the antitumor effects of α9‐nAChR‐specific antagonists, lead compounds ...
Urokinase plasminogen activator (uPA) contributes to atherosclerosis, restenosis and vascular remodeling. We have recently identified nAChRα1 as a functional cell receptor for uPA in addition to its classic receptor, uPAR. Here, we test the hypothesis that nAChRα1 plays a role in the pathogenesis of atherosclerosis. C57BL/6J ApoE−/− mice (male) were initially fed a Western diet for 8 wks. Plasmid DNA encoding scramble RNA (pScr) or siRNA (pSir2) for nAChRα1 was then injected into the mice (n=15) using an aortic hydrodynamic gene transfer protocol. Three mice from each group were sacrificed 7 days after DNA injection to confirm the nAChRα1 gene silencing. The rest of the mice continued on the Western diet for an additional 16 wks. Aortas were harvested for paraffin-embedding (aorta root), protein (ascending aorta and aortic arch) and RNA (descending aorta) (n=8). Whole aortas were isolated for oil red staining in 4 mice of each group. The nAChRα1 was highly up-regulated in aortic ...
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Endotoxemia induces the release of TNF-α from macrophages, as part of an inflammatory process. Acetylcholine and nicotine inhibit the release of TNF-α from macrophages in vitro, through activation of nicotinic receptors. In animals, vagal nerve stimulation inhibits the increase in plasma TNF-α induced by endotoxemia in vivo (for review, see Tracey KJ. Nature 2002;420:853). It is proposed that acetylcholine diffuses from parasympathetic nerve terminals in reticuloendothelial organs, to inhibit inflammatory cells. Wang et al. studied the receptor subtype that mediates these actions. Nicotinic acetylcholine receptors are a family of ligand-gated pentameric ion channels. In humans, 16 different subunits have been identified (α1-7, α9-10, β1-4, δ, ε, and γ), and pentameric receptors are formed by various combinations of these subunits. It is known that the acetylcholine-sensitive TNF-α response is blocked by α-bungarotoxin, a peptide antagonist that binds to α1, α7, and α9. Biding of ...
Anti-Nicotinic Acetylcholine Receptor alpha 7 antibody (ab10096) has been cited in 24 publications. References for Human, Mouse, Rat, Snail in ICC/IF, IF, IHC…
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The α7-nicotinic acetylcholine receptor (α7-nAChR) is a ligand-gated ion channel widely expressed in vertebrates and is associated with numerous physiological functions. As transmembrane ion channels, α7-nAChRs need to be expressed on the surface of the plasma membrane to function. The receptor has been reported to associate with proteins involved with receptor biogenesis, modulation of receptor properties, as well as intracellular signaling cascades and some of these associated proteins may affect surface expression of α7- nAChRs. The putative chaperone resistance to inhibitors of cholinesterase 3 (Ric-3) has been reported to interact with, and enhance the surface expression of, α7-nAChRs. In this study, we identified proteins that associate with α7-nAChRs when Ric-3 is expressed. Using α-bungarotoxin (α-bgtx), we isolated and compared α7-nAChR-associated proteins from two stably transfected, human tumor-derived cell lines: SH-EP1-hα7 expressing human α7-nAChRs and the
The effects and time course of a single injection of beta-bungarotoxin into E14 rat embryos were examined with an electron-microscopic study of development of the internal intercostal somatic nerve. Within 24 h of injection, axons in this nerve becam
1IDL: The solution structure of the complex formed between alpha-bungarotoxin and an 18-mer cognate peptide derived from the alpha 1 subunit of the nicotinic acetylcholine receptor from Torpedo californica.
rs1051730, also known as D398N, is a SNP in the nicotinic acetylcholine receptor alpha 3 subunit CHRNA3 gene. In two recent (2008) studies, together comprising over 6,000 lung cancer patients of European ancestry, the rs1051730(T) allele was very significantly associated with increased risk. Having one copy (i.e. being a rs1051730(C;T) genotype) increased risk for lung cancer about 1.3x, and having two copies (rs1051730(T;T) individuals) represented 1.8x increased risk. Up to 14% of lung cancer incidence may be attributable to this allele.[PMID 18385738, PMID 18385676] An independent study published at the same time concluded that (T) allele carriers for SNP rs1051730 are not at higher risk of becoming smokers compared to (C) carriers. However, if they do smoke, (T) carriers are quite likely to smoke more cigarettes than (C) carriers, and as an apparent consequence, they are at higher risk for lung cancer as reported in this and other studies. This study therefore links rs1051730 directly to ...
rs1051730, also known as D398N, is a SNP in the nicotinic acetylcholine receptor alpha 3 subunit CHRNA3 gene. In two recent (2008) studies, together comprising over 6,000 lung cancer patients of European ancestry, the rs1051730(T) allele was very significantly associated with increased risk. Having one copy (i.e. being a rs1051730(C;T) genotype) increased risk for lung cancer about 1.3x, and having two copies (rs1051730(T;T) individuals) represented 1.8x increased risk. Up to 14% of lung cancer incidence may be attributable to this allele.[PMID 18385738, PMID 18385676] An independent study published at the same time concluded that (T) allele carriers for SNP rs1051730 are not at higher risk of becoming smokers compared to (C) carriers. However, if they do smoke, (T) carriers are quite likely to smoke more cigarettes than (C) carriers, and as an apparent consequence, they are at higher risk for lung cancer as reported in this and other studies. This study therefore links rs1051730 directly to ...
TY - JOUR. T1 - Adult forms of nicotinic acetylcholine receptors are expressed in the absence of nerve during differentiation of a mouse skeletal muscle cell line. AU - Shepherd, Dawn. AU - Brehm, Paul. PY - 1994. Y1 - 1994. N2 - Changes in the functional properties of acetylcholine receptor (AchR) channels were followed in the C2 muscle cell line over the period of 1 to 17 days following myotube formation. Up to 1 week after myotube formation, the predominant class of channel exhibited low (45 pS) conductance and long mean channel open time (14 msec), characteristic of the major type of AchR in embryonic skeletal muscle. Three additional Ach-activated currents with conductances lower than 45 pS and long channel open times were also observed. Seven to 10 days following myotube formation, channels of 45 pS and 65 pS and short (2-6 msec) mean open duration were observed, characteristic of receptor channels in adult muscle. Increases in ε subunit mRNA levels preceded the functional expression of ...
Alpha6-containing nicotinic acetylcholine receptors are primarily within neurons from the midbrain dopaminergic (DA) system, recommending these receptors get excited about medicine pay back and dependence potentially. with bath program, however, not during intracellular administration, which inhibition isnt use-dependent. Additionally, in oocytes, cocaine both 6N/3C23-nAChRs and 6M211L/3IC23-nCAhRs inhibits likewise, recommending that cocaine may not respond over the 3 transmembrane domains of chimeric 6N/3C23-nAChR. In isolated VTA DA neurons mechanically, cocaine abolishes 6*-nAChR-mediated improvement of spontaneous inhibitory postsynaptic currents (sIPSCs). Collectively, these research supply the initial evidence that cocaine inhibits the function of both heterologously and naturally portrayed 6*-nAChRs directly. These findings claim that 6*-nAChRs might provide a book pharmacological focus on mediating the consequences of cocaine and could underlie a book system of cocaine incentive and ...
0020] Conventionally, it is known that an anti-VGKC complex antibody relates to Isaacs syndrome of which the number of patients is extremely few. Therefore, the development of a diagnostic agent of anti-VGKC complex antibody has not progressed. On the other hand, as indicated in Examples, the anti-VGKC complex antibody is specifically expressed in a certain patient with fibromyalgia. Therefore, the anti-VGKC complex antibody becomes a specific marker of fibromyalgia. On the other hand, a reagent for directly detecting the anti-VGKC complex antibody has not been developed at this moment. Thus, bungarotoxin that is a potassium channel inhibitor is made to be bound to a VGKC. As a result, a complex consisting of a VGKC and bungarotoxin; or a complex containing a VGKC, a protein bound to a VGKC, and bungarotoxin is obtained. Therefore, by using an antibody against bungarotoxin, a VGKC complex may be detected. That is, the level of VGKC complex may be measured by using the level of the antibody ...
Dissorophus (DI-soh-ROH-fus) is an extinct genus of the early temnospondyl amphibian families that flourished in the Late Carboniferous to the Late Permian, 273 million years ago. Most recent discovery of the Dissorophus species is D. multicinctus. Their remains have been found in the Northern and Central Texas, and distinguished from other members of its clade by its small body size, disproportionately large head and short trunk. Dermal ossification in the sacral region and skull suggests that D. multicinctus are among the non-amniotes that were successful on land. The name dissorphus was used by Edward Drinker Cope to describe the first dissorophid, Dissorophus multicinctus. He did not formulate a standing definition as of this name, however, upon examination, he commented that it was a veritable bratrachian armadillo which translates to looking like an amphibian armadillo. On the same context,DeMar [3] mentions that Boulengers interpretation on dissorophus is remarkable for an ...
The function of Ric-3, which is required for nicotinic acetylcholine receptor (nAChR) expression in C. elegans, is unclear. Here we found that Ric-3 can promote or inhibit cell-surface delivery of alpha-bungarotoxin-binding nAChRs (BgtRs) composed of alpha7 subunits. At low levels, Ric-3 promoted BgtR assembly, endoplasmic reticulum (ER) release, and cell-surface delivery without trafficking from the ER. At high Ric-3 levels, Ric-3 suppressed BgtR surface delivery, but not its assembly, and BgtRs were retained in the ER or in Ric-3-containing aggregates. In PC12 cells, native BgtRs trafficked to the cell surface from the ER where low levels of endogenous Ric-3 were observed. In cultured neurons, native Ric-3 levels were higher than in PC12 cells, and Ric-3 and alpha7 subunits were found in somata and dendrites, but not axons, of inhibitory interneurons. Ric-3 trafficked with alpha7 subunits in rapidly moving vesicles to dendrites, where it was restricted to the ER subcompartment. We conclude ...
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Deloukas P, Matthews LH, Ashurst J, Burton J, Gilbert JG, Jones M, Stavrides G, Almeida JP, Babbage AK, Bagguley CL, Bailey J, Barlow KF, Bates KN, Beard LM, Beare DM, Beasley OP, Bird CP, Blakey SE, Bridgeman AM, Brown AJ, Buck D, Burrill W, Butler AP, Carder C, Carter NP, Chapman JC, Clamp M, Clark G, Clark LN, Clark SY, Clee CM, Clegg S, Cobley VE, Collier RE, Connor R, Corby NR, Coulson A, Coville GJ, Deadman R, Dhami P, Dunn M, Ellington AG, Frankland JA, Fraser A, French L, Garner P, Grafham DV, Griffiths C, Griffiths MN, Gwilliam R, Hall RE, Hammond S, Harley JL, Heath PD, Ho S, Holden JL, Howden PJ, Huckle E, Hunt AR, Hunt SE, Jekosch K, Johnson CM, Johnson D, Kay MP, Kimberley AM, King A, Knights A, Laird GK, Lawlor S, Lehvaslaiho MH, Leversha M, Lloyd C, Lloyd DM, Lovell JD, Marsh VL, Martin SL, McConnachie LJ, McLay K, McMurray AA, Milne S, Mistry D, Moore MJ, Mullikin JC, Nickerson T, Oliver K, Parker A, Patel R, Pearce TA, Peck AI, Phillimore BJ, Prathalingam SR, Plumb RW, Ramsay H, ...
Although a fair number of genes coding for neuronal nAChRs have already been identified it is clear that reconstitution experiments have failed to describe all the subtypes observed in native cells (Pugh et al., 1995; Sorenson and Gallagher, 1996; Cuevas and Berg, 1998). The sequencing of the full genome of the nematode Caenorhabditis elegans has revealed the existence of over 40 potential genes encoding nicotinic acetylcholine receptor subunits in this organism (Littleton and Ganetzky, 2000), whereas to date only 16 nAChR subunits have been cloned in vertebrates (Lindstrom, 1997). Thus, yet undiscovered subunit could account for the existence of novel receptor proteins. In this work, we present evidence for the existence of a new nAChR subtype that would be composed by the association of α9 with a novel α10-subunit.. When expressed in X. laevis oocytes, the human α9-subunit was able to form recombinant homomeric channels activated by acetylcholine with properties similar to those reported ...
The Laboratory of Neurochemistry focuses on nicotinic acetylcholine receptors critical to chemical signaling and electrical wiring in the brain. Read more.
Since 2004, there has been an increasing body of evidence that points to defects in the NMJ as one of the primary pathological events in ALS (Fischer et al., 2004; Dupuis et al., 2009). The T70I model exhibits early abnormalities at the NMJ. At 11 dpf there is a significant reduction in colocalisation of α-bungarotoxin and SV2 in the interseptal region, between homozygous T70I sod1 zebrafish and their WT and heterozygous clutch mates. This observation might be due to either a failure of the NMJs to form correctly during embryogenesis, or due to a later disruption of the NMJ, followed by the dying back of the axon. Further investigation will be required to determine which of these mechanisms is operating. Our data are consistent with evidence from other studies that point to NMJ alteration as an early pathogenic event and support the validity of the T70I zebrafish model (Fischer et al., 2004; Dupuis et al., 2009; Dupuis and Loeffler, 2009; Ramesh et al., 2010).. It should be noted, however, that ...
A 125I-bungarotoxin labelling study of the acetylcholine receptor on the nerve-muscle junctions in the course of aging in the rat is reported. Attention is drawn to the fact that aging leads to an appreciable slowing down of the receptor degradation time, whereas no change occurs in its location.
AP reaches teminal of MN→ Ca++ influx occurs via volt-gated Ca++ channels → synaptic ACh excytosis (1 vesicle = 10,000 molecules of ACh) → ACh diffuses to junct. folds, binds nicotinic AChR → depolarization (endplate potential) ...
TY - JOUR. T1 - Alpha 4-2 beta 2 and other nicotinic acetylcholine receptor subtypes as targets of psychoactive and addictive drugs. AU - Connolly, John. AU - Boulter, Jim. AU - Heinemann, Stephen F.. PY - 1992/3. Y1 - 1992/3. N2 - 1. Xenopus oocytes were injected with various muscle and neuronal nicotinic acetylcholine receptor (ACh receptor, cholinoceptor) subunit RNA combinations and their pharmacological properties studied using two-electrode voltage clamp. The functional expression of one of these combinations, rat alpha 4-2 beta 2, has not been previously described. The alpha 4-2 mRNA is a splicing variant transcribed from the alpha 4 gene. In the experiments reported here, the alpha 4-2 beta 2 subtype was functionally indistinguishable from the alpha 4-1 beta 2 subtype. 2. For each subtype, the relative potency of nicotine compared with acetylcholine was obtained by estimating the relative concentration of nicotine which would elicit the same current response as 0.1 microM Ach. The ratios ...
It is well established that nicotinic receptors in the mammalian striatum are involved in modulation of the release of several neurotransmitters, including dopamine. In addition, nicotinic receptors with high affinity for agonists have generally been found to be reduced in the striatum in Parkinsons disease. In the present study antibodies have been used to examine which subunits contribute to the striatal nicotinic receptor loss in Parkinsons disease, and whether the reduction in [(3)H]nicotine binding correlates with synaptic loss. Autopsy tissue from the putamen of 12 Parkinsons disease cases and 12 age-matched control subjects was analysed by immunoblotting using antibodies against recombinant peptides specific for alpha3, alpha4, alpha7, beta2 and beta4 nicotinic acetylcholine receptor (nAChR) subunits and the synaptic marker synaptophysin, in conjunction with assessment of [(3)H]nicotine binding by autoradiography. The data indicate that there is no loss of alpha3, alpha4, alpha7 and beta2
Genetic mutations responsible for CMSs have been identified in relation to proteins in the presynaptic, synaptic and postsynaptic compartments of the neuromuscular endplate. As expected, the frequency of particular gene mutations varies within different ethnic groups, but in most populations the most common form of CMS is due to a deficiency of acetylcholine receptors on the postsynaptic membrane [3]. These can result from recessive missense, nonsense, frameshift or splice site and promoter region mutations in any of the genes encoding the acetylcholine receptor subunits. However, a high frequency of mutations in the acetylcholine receptor ε subunit (CHRNE) compared with other subunits has been recognised and attributed to the phenotypic rescue by maintained low level expression of the foetal γ subunit that substitutes for the defective ε subunit, but cannot compensate for the other muscle acetylcholine receptor subunits. Our patient was diagnosed with c.183_187dupCTCAC within CHRNE, which is ...
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular ...
This gene encodes a nicotinic acetylcholine receptor, which belongs to a superfamily of ligand-gated ion channels that play a role in fast signal transmission at synapses. These pentameric receptors can bind acetylcholine, which causes an extensive change in conformation that leads to the opening of an ion-conducting channel across the plasma membrane. This protein is an integral membrane receptor subunit that can interact with either nAChR beta-2 or nAChR beta-4 to form a functional receptor. Mutations in this gene cause nocturnal frontal lobe epilepsy type 1. Polymorphisms in this gene that provide protection against nicotine addiction have been described. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2012 ...
We have investigated the topology of the alpha and delta subunits of the nicotinic acetylcholine receptor (AChR) from mammalian muscle synthesized in an in vitro translation system supplemented with dog pancreatic microsomes. Fusion proteins were expressed in which a carboxy-terminal fragment of bovine prolactin was attached downstream of each of the major putative transmembrane domains, M1-M4 and MA, in the AChR subunits. The orientation of the prolactin domain relative to the microsomal membrane was then determined for each protein by a proteolysis protection assay. Since the prolactin domain contains no information which either directs or prevents its translocation, its transmembrane orientation depends solely on sequences within the AChR subunit portion of the fusion protein. When subunit-prolactin fusion proteins with the prolactin domain fused after either M2 or M4 were tested, prolactin-immunoreactive peptides that were larger than the prolactin domain itself were recovered. No ...
Background: The frequent co-abuse of alcohol and tobacco may suggest that they share some common neurological mechanisms. For example, nicotine acts on Nicotinic acetylcholine receptors (nAChRs) in the brain to release dopamine to sustain addiction. Might nAChRs be entwined with alcohol? Objectives: This review summarizes recent studies on the relationship between alcohol and nAChRs, including the role of nAChRs in molecular biological studies, genetic studies and pharmacological studies on alcohol, which indicate that nAChRs have been potently modulated by alcohol. Methods: We performed a cross-referenced literature search on biological, genetic and pharmacological studies of alcohol and nAChRs. Results: Molecular biological and genetic studies indicated that nAChR (genes) may be important in mediating alcohol intake, but we still lack substantial evidence about how it works. Pharmacological studies proved the correlation between nAChRs and alcohol intake, and the association between nicotine and
The effects of mast cell degranulating peptide (MCDP), a toxin from the honey bee, and of dendrotoxin (DTX), a toxin from the green mamba snake, were studied in voltage-clamped experiments with myelinated nerve fibres of Xenopus. MCDP and DTX blocked part of the K+ current. About 20% of the K+ current, however, was resistant to the toxins even in high concentrations. In Ringer solution half-maximal block was reached with concentrations of 33 nM MCDP and 11 nM DTX. In high-K+ solution the potency of both toxins was lower. β-Bungarotoxin (β-BuTX), another snake toxin, also blocked part of the K+ current, but was less potent than MCDP and DTX. Tail currents in high-K+ solution were analysed and three K+ current components were separated according to Dubois (1981b). Both MCDP and DTX selectively blocked a fast deactivating, slowly inactivating K+ current component which steeply activates between E = -60 mV and E = -40 mV (component f1). In concentrations around 100 nM, MCDP and DTX blocked neither ...
In a two-electrode voltage-clamp study on the rat sympathetic neuron, the properties of the subsynaptic native neuronal AChR (nAChR) in response to the physiologically released ACh were shown to be modified within a few hours after denervation (Sacchi et al., 2008), suggesting that the nAChR ion selectivity switched from preferential permeability to potassium ions to scarce selectivity between K+ and Na+; the changes regarded synaptic, but not extrasynaptic, receptors and revealed an unexpected flexibility of the nicotinic channel in its permeation properties. Subsequently, a number of quite simple experimental procedures in intact ganglia were also shown to produce changes in conductance and ion selectivity properties of the nAChR; unlike denervation, such procedures (resting membrane potential shifts within a voltage range of physiological interest, ionic modifications, and the action of α-bungarotoxin) were very unlikely to acutely produce modifications in nAChR subunit composition or steric ...
The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha subunits and 1 each of the beta, gamma, and delta subunits. This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Nov 2012 ...
We contrast the phenotypes associated with hereditary acetylcholine receptor deficiency arising from mutations in either the acetylcholine receptor epsilon subunit or the endplate acetylcholine receptor clustering protein rapsyn. Mutational screening was performed by amplification of promoter and co …
The first recordings from individual ion channels were achieved using the patch-clamp to measure currents through muscle nicotinic acetylcholine receptor/channels (Neher and Sakmann 1976); a technique that subsequently revolutionized studies of channel function and biophysics (Hamill et al., 1981; Hille 2001). Here, we demonstrate the use of optical techniques to obtain analogous physiological information from these same channels, by imaging single-channel Ca2+ flux (SCCaFTs) as a reporter of channel gating. One major advantage over electrophysiological recording is that optical single-channel imaging is massively parallel, providing simultaneous readout from hundreds of channels (Fig. 3). This enormously enhanced dataset should facilitate detailed statistical analysis of Markovian channel behavior. For example, we had shown that N-type channels within the same optical field display divergent open probabilities, with individual channels displaying transitions between low and high frequency ...
Nicotinic Acetylcholine Receptor beta小鼠单克隆抗体[B3](ab11150)可与人样本反应并经WB, IP, IHC, Flow Cyt实验严格验证,被5篇文献引用。
When compared in nAChR-binding studies, MLA was found to compete for 125I-α-bungarotoxin binding sites (i.e. α7 sub-types) over ... Subsequently, Macallan and his co-workers showed that MLA also competed with 125I-α-bungarotoxin (Ki ~1 x 10−9M) and tritiated ... These workers also reported that MLA displaced125I-α-bungarotoxin from purified Torpedo (electric ray) nicotinic acetylcholine ... but its affinity for 125I-α-bungarotoxin binding sites is over 200x lower than that of MLA. If the -NH2 group of ...
... known as α-bungarotoxins and β-bungarotoxins, among others). By weight, almost half of the protein content of the venom is ... α-Bungarotoxin is important for neuromuscular histology, it is known to bind irreversibly to receptors of the neuromuscular ... composed of β-bungarotoxins. The average venom yield from specimens kept on snake farms is about 4.6 mg-19.4 mg per bite. The ...
In 1963, Lee worked with Chang Chuan-chung (張傳炯), a chemist, and separated the deadly α-type and β-type bungarotoxins of the ...
Following envenomation with bungarotoxins, transmitter release is initially blocked (leading to a brief paralysis), followed by ...
... α-bungarotoxin from cobras). As with plant feeding deterrents, this biological activity is attributed to natural selection, ...
... and that one or two molecules of α-bungarotoxin (or other long-chain α-neurotoxin) suffice to halt this motion. The toxins seem ...
β-Bungarotoxin; Acetylcholine release inhibitors: Botulinum toxin (Botox); Acetylcholinesterase reactivators: Asoxime. * ...
"Alpha-bungarotoxin Binding to Target Cell in a Developing Visual System by Carboxylated Nanodiamond." Nanotechnology, 19 (20): ...
... (CTX III, also known as cytotoxin 3) is a sixty amino-acid polypeptide toxin from the Taiwan Cobra Naja atra. It is an example of a group of snake cardio/cytotoxins (InterPro: IPR003572), which are made up of shorter snake venom three-finger toxins.[1] Recent evidence has shown that CTX III may induce apoptosis in K562 cells via the release of cytochrome c.[2] ...
No animal species is immune to the acute toxic effects of aflatoxins. Adult humans have a high tolerance for aflatoxin exposure and rarely succumb to acute aflatoxicosis,[23] but children are particularly affected, and their exposure can lead to stunted growth and delayed development, in addition to all the symptoms mentioned below.[4] High-level aflatoxin exposure produces an acute hepatic necrosis (acute aflatoxicosis), resulting later in cirrhosis or carcinoma of the liver. Acute liver failure is made manifest by bleeding, edema, alteration in digestion, changes to the absorption and/or metabolism of nutrients, and mental changes and/or coma.[23] Chronic, subclinical exposure does not lead to symptoms so dramatic as acute aflatoxicosis. Chronic exposure increases the risk of developing liver and gallbladder cancer,[24] as aflatoxin metabolites may intercalate into DNA and alkylate the bases through epoxide moiety. This is thought to cause mutations in the p53 gene, an important gene in ...
... only affects mammals. No effect is found on reptiles, insects or fish. In experiments performed on mice, symptoms such as convulsions, continuous urination, tremors and tachypnea occurred 10 minutes after injection and increased during 30 minutes. An injection of 1 μg of birtoxin resulted in severe neurotoxic effects for 24 hours, but this dose is not lethal to mice. LD99 in mice is achieved at 2 μg.[1]. An antibody against the N-terminus of the birtoxin protein structure has been shown to neutralize the venom of the South African spitting scorpion, and such antibodies may be useful clinically to treat envenomation.[9]. ...
In general, when scientists determine the amount of a substance that may be hazardous for humans, animals and/or the environment they determine the amount of the substance likely to trigger effects and if possible establish a safe level. In Europe, the European Food Safety Authority produced risk assessments for more than 4,000 substances in over 1,600 scientific opinions and they provide open access summaries of human health, animal health and ecological hazard assessments in their: OpenFoodTox[22] database. [23][24] The OpenFoodTox database can be used to screen potential new foods for toxicity.[25] The Toxicology and Environmental Health Information Program (TEHIP)[26] at the United States National Library of Medicine (NLM) maintains a comprehensive toxicology and environmental health web site that includes access to toxins-related resources produced by TEHIP and by other government agencies and organizations.[27] This web site includes links to databases, bibliographies, tutorials, and other ...
The first three steps outline the travel of tetanus from the peripheral nervous system to where it is taken up to the CNS and has its final effect. The last three steps document the changes necessary for the final mechanism of the neurotoxin. Transport to the CNS inhibitory interneurons begins with the B-chain mediating the neurospecific binding of TeNT to the nerve terminal membrane. It binds to GT1b polysialogangliosides, similarly to the botulinum neurotoxin. It also binds to another poorly characterized GPI anchored protein receptor more specific to TeNT.[10][11] Both the ganglioside and the GPI anchored protein are located in lipid microdomains and both are requisite for specific TeNT binding.[11] Once it is bound the neurotoxin is then endocytosed into the nerve and begins to travel through the axon to the spinal neurons. The next step, transcytosis from the axon into the CNS inhibitory interneuron, is one of the least understood parts of TeNT action. At least two pathways are involved, ...
Glutamate is the most abundant excitatory neurotransmitter in the vertebrate nervous system.[21] At chemical synapses, glutamate is stored in vesicles. Nerve impulses trigger release of glutamate from the presynaptic cell. Glutamate acts on ionotropic and metabotropic (G-protein coupled) receptors.[21] In the opposing postsynaptic cell, glutamate receptors, such as the NMDA receptor or the AMPA receptor, bind glutamate and are activated. Because of its role in synaptic plasticity, glutamate is involved in cognitive functions such as learning and memory in the brain.[22] The form of plasticity known as long-term potentiation takes place at glutamatergic synapses in the hippocampus, neocortex, and other parts of the brain. Glutamate works not only as a point-to-point transmitter, but also through spill-over synaptic crosstalk between synapses in which summation of glutamate released from a neighboring synapse creates extrasynaptic signaling/volume transmission.[23] In addition, glutamate plays ...
... acts by the following mechanism: First, the B subunit ring of the cholera toxin binds to GM1 gangliosides on the surface of target cells. The B subunit can also bind to cells lacking GM1. The toxin then most likely binds to other types of glycans, such as Lewis Y and Lewis X, attached to proteins instead of lipids.[7][8][9] Once bound, the entire toxin complex is endocytosed by the cell and the cholera toxin A1 (CTA1) chain is released by the reduction of a disulfide bridge. The endosome is moved to the Golgi apparatus, where the A1 protein is recognized by the endoplasmic reticulum chaperone, protein disulfide isomerase. The A1 chain is then unfolded and delivered to the membrane, where Ero1 triggers the release of the A1 protein by oxidation of protein disulfide isomerase complex.[10] As the A1 protein moves from the ER into the cytoplasm by the Sec61 channel, it refolds and avoids deactivation as a result of ubiquitination. CTA1 is then free to bind with a human partner protein ...
... occludes the pore of calcium-activated voltage-gated shaker K+ channels by binding to one of four independent, overlapping binding sites.[6][7] It binds both to the open and the closed states. In addition, the block is enhanced as the ionic strength is lowered.[8] This block occurs as the Asn 30 on the CTX interacts with the Asp 381 on the K+ channel.[9] The blockade of K+ channels by the charybdotoxin peptide causes neuronal hyperexcitability. Mutations of the Lys31Gln and the Asn30Gln had the effect of lessening the CTX block of the pore on the shaker channel.[9] ...
LPS acts as the prototypical endotoxin because it binds the CD14/TLR4/MD2 receptor complex in many cell types, but especially in monocytes, dendritic cells, macrophages and B cells, which promotes the secretion of pro-inflammatory cytokines, nitric oxide, and eicosanoids.[16] As part of the cellular stress response, superoxide is one of the major reactive oxygen species induced by LPS in various cell types that express TLR (toll-like receptor). LPS is also an exogenous pyrogen (fever-inducing substance). Being of crucial importance to Gram-negative bacteria, these molecules make candidate targets for new antimicrobial agents. Some researchers doubt reports of generalized toxic effects attributed to all lipopolysaccharides, in particular, for cyanobacteria.[17] LPS function has been under experimental research for several years due to its role in activating many transcription factors. LPS also produces many types of mediators involved in septic shock. Humans are much more sensitive to LPS than ...
Symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity),[1] vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea. Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart). Quinine may also trigger a rare form of hypersensitivity reaction in malaria patients, termed blackwater fever, that results in massive hemolysis, hemoglobinemia, hemoglobinuria, and kidney failure.[citation needed] Most symptoms of cinchonism (except in severe cases) are reversible and disappear once quinine is withdrawn. ...
... is a condition or a process in which an organism becomes chemically harmed severely (poisoned) by a toxic substance or venom of an animal.[1] Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning. Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not ...
In biology, poisons are substances that cause disturbances in organisms, usually by chemical reaction or other activity on the molecular scale, when an organism absorbs a sufficient quantity.[1][2] The fields of medicine (particularly veterinary) and zoology often distinguish a poison from a toxin, and from a venom. Toxins are poisons produced by organisms in nature, and venoms are toxins injected by a bite or sting (this is exclusive to animals). The difference between venom and other poisons is the delivery method. Industry, agriculture, and other sectors employ poisonous substances for reasons other than their toxicity. Most poisonous industrial compounds have associated material safety data sheets and are classed as hazardous substances. Hazardous substances are subject to extensive regulation on production, procurement and use in overlapping domains of occupational safety and health, public health, drinking water quality standards, air pollution and environmental protection. Due to the ...
... includes four (4) syndromes that share some common features and are primarily associated with bivalve molluscs (such as mussels, clams, oysters and scallops.)[1] These shellfish are filter feeders and, therefore, accumulate toxins produced by microscopic algae, such as cyanobacteria, diatoms and dinoflagellates. ...
... (DSP) is one of the four recognized symptom types of shellfish poisoning, the others being paralytic shellfish poisoning, neurotoxic shellfish poisoning and amnesic shellfish poisoning. As the name suggests, this syndrome manifests itself as intense diarrhea and severe abdominal pains. Nausea and vomiting may sometimes occur too. DSP and its symptoms usually set in within about half an hour of ingesting infected shellfish, and last for about one day. A recent case in France, though, with 20 people consuming oysters manifested itself after 36 hours. The causative poison is okadaic acid, which inhibits intestinal cellular de-phosphorylation.[1] This causes the cells to become very permeable to water and causes profuse, intense diarrhea with a high risk of dehydration. As no life-threatening symptoms generally emerge from this, no fatalities from DSP have ever been recorded. ...
Zinc has been used therapeutically at a dose of 150 mg/day for months and in some cases for years, and in one case at a dose of up to 2000 mg/day zinc for months.[7][8][9][10][11] A decrease in copper levels and hematological changes have been reported; however, those changes were completely reversed with the cessation of zinc intake.[9] However, zinc has been used as zinc gluconate and zinc acetate lozenges for treating the common cold[12] and therefore the safety of usage at about 100 mg/day level is a relevant question. Thus, given that doses of over 150 mg/day for months to years has caused no permanent harm in many cases, a one-week usage of about 100 mg/day of zinc in the form of lozenges would not be expected to cause serious or irreversible adverse health issues in most persons. Unlike iron, the elimination of zinc is concentration-dependent.[13] ...
Others: Bungarotoxins (β-bungarotoxin, γ-bungarotoxin). Enhancers. *LPHN agonists: α-Latrotoxin. *Others: Atracotoxins (e.g., ...
Since characterization, the development of synthetic pathways to histrionicotoxin has been of interest to research groups due to its unusual functionality. The Kishi group proposed the first total synthesis of the parent 283A in 1985 using 89, a previously synthesized lactam used for the synthesis of other variants.[8] Treatment with acetic anhydride yielded 133 in quantitative yield. The cyclic enol ether 134 was formed through oxidative cleavage promoting intramolecular addition followed by a basic deprotection and dehydration. Bromination followed by dehydrobromination in methanol was then found to give an epimeric mixture of unsaturated 135. Hydrolysis, reduction and acetylation yielded 136. Formation of a thiolactam followed by condensation with ethyl bromoacetate gave 137. Selective deprotection of the allylic alcohol followed by oxidation gave 138. A Wittig reaction then generated a chloroalkene, which, upon base-promoted elimination of HCl, gave a terminal alkyne, which was subsequently ...
Others: Bungarotoxins (β-bungarotoxin, γ-bungarotoxin). Enhancers. *LPHN agonists: α-Latrotoxin. *Others: Atracotoxin (e.g., ...
Reproduction occurs generally between December and early May[citation needed]. Typically, the adult newts will return to the pool in which they hatched. After a mating dance, the male mounts the female and rubs his chin on her nose. He then attaches a spermatophore to the substrate, which she will retrieve into her cloaca.. The egg mass released by the female contains between seven and 30 eggs, and is roughly the consistency of a thick gelatin dessert[citation needed]. Typically, the egg masses are attached to stream plant roots or to rocky crevices in small pools of slow-moving water, but they have also been known to be attached to underwater rocks or leaf debris. While shallow in a wide sense, these pools are rather deep relative to the average depth of a Southern California stream, varying in depth from about 1-2 metres (3.3-6.6 ft).. Adult newts typically leave the pools shortly after breeding has concluded, however, some adults may remain in the pools for an additional few months to ...
... s are often distinguished from other chemical agents by their method of production-the word toxin does not specify method of delivery (compare with venom and the broader meaning of poison-all substances that can also cause disturbances to organisms). It simply means it is a biologically produced poison. There was an ongoing terminological dispute between NATO and the Warsaw Pact over whether to call a toxin a biological or chemical agent, in which the NATO opted for biological agent, and the Warsaw Pact, like most other countries in the world, for chemical agent.[citation needed] According to an International Committee of the Red Cross review of the Biological Weapons Convention, "Toxins are poisonous products of organisms; unlike biological agents, they are inanimate and not capable of reproducing themselves", and "Since the signing of the Constitution, there have been no disputes among the parties regarding the definition of biological agents or toxins".[4] According to Title 18 of the ...
The heat-labile enterotoxin is inactivated at high temperatures.[1][2]. It acts similarly to the cholera toxin by raising cAMP levels through ADP-ribosylation of the alpha-subunit of a Gs protein leading to the constitutive activation of adenylate cyclase. Elevated cAMP levels stimulate the activation of the CFTR channel thus stimulating secretion of chloride ions and water from the enterocyte into the gut lumen. This ionic imbalance causes watery diarrhea.. In addition to its effects on chloride secretion, which involve the same steps as the effects of cholera toxin, heat-labile enterotoxin binds additional substrates: lipopolysaccharide on the surface of E. coli cells and A-type blood antigens.[3] The importance of these binding events is not yet known.. ...
... bungarotoxin, CF633 \ 00009 for more molecular products just contact us ... We have also other products like : alpha_bungarotoxin, CF633. Related products : alpha_bungarotoxin, CF633 ...
Morley, B. J., & Garner, L. L. (1986). Increases in the concentration of brain α-bungarotoxin binding sites induced by dietary ... Morley, Barbara J. ; Garner, Laura L. / Increases in the concentration of brain α-bungarotoxin binding sites induced by dietary ... Increases in the concentration of brain α-bungarotoxin binding sites induced by dietary choline are age-dependent. / Morley, ... Fingerprint Dive into the research topics of Increases in the concentration of brain α-bungarotoxin binding sites induced by ...
... alpha-bungarotoxin (alpha BgTX) binding sites that correspond to alpha 7-type nAChR in mammalian brain. We have shown that, ... Nudicauline and elatine as potent norditerpenoid ligands at rat neuronal alpha-bungarotoxin binding sites: importance of the 2 ... Nudicauline and elatine as potent norditerpenoid ligands at rat neuronal alpha-bungarotoxin binding sites: importance of the 2 ... Nudicauline and elatine as potent norditerpenoid ligands at rat neuronal alpha-bungarotoxin binding sites: importance of the 2 ...
β-Bungarotoxin-induced phospholipid hydrolysis in rat brain synaptosomes: effect of replacement of calcium by strontium. ... β-Bungarotoxin-induced phospholipid hydrolysis in rat brain synaptosomes: Effect of replacement of calcium by strontium. * ... β-Bungarotoxin-induced phospholipid hydrolysis in rat brain synaptosomes: effect of replacement of calcium by strontium. ... We tested whether, upon substitution of Ca2+by Sr2+in a medium containing β-bungarotoxin, sufficient Ca2+remained bound to the ...
Neuronal bungarotoxin has previously been shown, using two-dimensional 1H NMR spectroscopy, to have a triple-stranded ... Neuronal bungarotoxin has previously been shown, using two-dimensional 1H NMR spectroscopy, to have a triple-stranded ... An approach was therefore adopted which produced model structures based to varying degrees on the alpha-bungarotoxin structure ... Solution structure of neuronal bungarotoxin determined by two-dimensional NMR spectroscopy: calculation of tertiary structure ...
The effects and time course of a single injection of beta-bungarotoxin into E14 rat embryos were examined with an electron- ... Bungarotoxins / toxicity*. Embryo, Mammalian / drug effects. Embryonic and Fetal Development / drug effects. Female. Microscopy ... beta-Bungarotoxin applied on E17 destroyed developing axons in a similar manner, but the perineurium remained in place, and ... The effects and time course of a single injection of beta-bungarotoxin into E14 rat embryos were examined with an electron- ...
... bungarotoxin explanation free. What is bungarotoxin? Meaning of bungarotoxin medical term. What does bungarotoxin mean? ... Looking for online definition of bungarotoxin in the Medical Dictionary? ... bungarotoxin. bungarotoxin. One of three (alpha, beta, gamma) closely related anticholinergic neurotoxins derived from venom of ... Bungarotoxin , definition of bungarotoxin by Medical dictionary https://medical-dictionary.thefreedictionary.com/bungarotoxin ...
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
Basic phospholipase A2 beta-bungarotoxin A2 chainAdd BLAST. 120. Amino acid modifications. Feature key. Position(s). ... sp,Q8QFW3,PA2B2_BUNCE Basic phospholipase A2 beta-bungarotoxin A2 chain OS=Bungarus caeruleus OX=132961 PE=2 SV=1 ... Basic phospholipase A2 beta-bungarotoxin A2 chain (EC:3.1.1.4). Short name: ...
Basic phospholipase A2 beta-bungarotoxin A2 chainAdd BLAST. 119. Amino acid modifications. Feature key. Position(s). ... sp,Q7T1R1,PA2B2_BUNFL Basic phospholipase A2 beta-bungarotoxin A2 chain OS=Bungarus flaviceps flaviceps OX=8615 PE=1 SV=1 ... Basic phospholipase A2 beta-bungarotoxin A2 chain (EC:3.1.1.4). Short name: ...
Our bright and photostable Alexa Fluor 647 -bungarotoxin may prove to be one of the best probes for v ... Bungarotoxin, a 74-amino acid peptide extracted from Bungarus multicinctus venom, binds with high affinity to the -subunit of ... α-Bungarotoxin, a 74-amino acid peptide extracted from Bungarus multicinctus venom, binds with high affinity to the α-subunit ... Our bright and photostable Alexa Fluor® 647 α-bungarotoxin may prove to be one of the best probes for visualizing this receptor ...
α-Bungarotoxin, CF® Dye and Other Conjugates Conjugates of α-Bungarotoxin labeled with a selection of our CF® dyes and other ... Biotin-XX-α-Bungarotoxin Biotinylated α-bungarotoxin is useful in the affinity column isolation of the nicotinic AChR using an ... We also offer unlabeled α-bungarotoxin and CF® Dye α-Bungarotoxin conjugated to our next-generation fluorescent dyes. See our ... Biotinylated α-bungarotoxin is useful in the affinity column isolation of the nicotinic AChR using an avidin or streptavidin ...
Absence of [125I] alpha-bungarotoxin binding to motor nerve terminals of frog, lizard and mouse muscle. SW Jones and MM ... We have re- examined this issue by electron microscope autoradiography with [125I] alpha-bungarotoxin, following separation of ... Absence of [125I] alpha-bungarotoxin binding to motor nerve terminals of frog, lizard and mouse muscle ... We conclude that there are essentially no presynaptic acetylcholine receptors that bind alpha-bungarotoxin at vertebrate ...
1995) α-Bungarotoxin receptor subtypes. in Effects of nicotine on biological systems, Pt II, eds Clarke PBS, Quik M, Adlkofer F ... 1989) [125I]α-bungarotoxin binding marks primary sensory areas of developing rat neocortex. Brain Res 501:223-234. ... 1986) α-Bungarotoxin binds to low-affinity nicotine binding sites in rat brain. J Neurochem 47:1706-1712. ... 1990) Brain α-bungarotoxin binding protein cDNAs and mAbs reveal subtypes of this branch of the ligand-gated ion channel gene ...
The dynamic of Trp residue in Β1-bungarotoxin ( gb1-Bgt), the A chain of Β1-Bgt and phospholipase A2 (PLA2) was assessed by ... The dynamic of Trp residue inΒ1-bungarotoxin (gb1-Bgt), the A chain ofΒ1-Bgt and phospholipase A2 (PLA2) was assessed by ... The essentiality of B chain in stabilizing the structure of the A chain in β1-bungarotoxin fromBungarus multicinctus venom. ... Snake venom Trp fluorescence Β1-bungarotoxin role of the B chain ...
α-Bungarotoxin, CF® Dye and Other Conjugates Conjugates of α-Bungarotoxin labeled with a selection of our CF® dyes and other ... We also offer Biotin-XX-alpha-bungarotoxin (catalog. no. 00017), and unconjugated alpha-bungarotoxin.(catalog no. 00010-1). See ... Alpha-bungarotoxin is a polypeptide snake toxin that binds to the nicotinic acetylcholine receptor found at the neuromuscular ... Labeled α-bungarotoxin conjugates can be used for staining nicotinic acetylcholine receptors at neuromuscular junctions in ...
... alpha-bungarotoxin from alpha7 nAChR in C57BL/6J mouse hippocampal membrane. ...
The cDNA encoding the A chain ofΒ-bungarotoxin (Β-Bgt) was constructed from the cellular RNA isolated from the venom glands ... The cDNA encoding the A chain ofΒ-bungarotoxin (Β-Bgt) was constructed from the cellular RNA isolated from the venom glands of ... A chain ofΒ-bungarotoxin cDNA sequence analysis mutagenesis of cysteine residues refolding of the recombinant A chain ... cDNA sequence analysis and mutagenesis studies on the a chain of Β-bungarotoxin from Taiwan banded krait. ...
α-bungarotoxin. CNS. central nervous system. GABA. γ-amino butyric acid. MEM. minimum essential medium. HEPES. (N-[2- ... 1990) Brain α-bungarotoxin binding protein, cDNAs and MAbs reveal subtypes of this branch of the ligand-gated ion channel gene ... Strychnine (2 μM) decreased the peak amplitude of the α-bungarotoxin-sensitive type IA current in a voltage-independent manner ... 1996) α-Conotoxin-ImI: A competitive antagonist at α-bungarotoxin-sensitive neuronal nicotinic receptors in hippocampal neurons ...
Membrane-bound α-bungarotoxin-binding entities derived from rat brain are found to interact specifically with the affinity ... Interaction of Nicotinic Receptor Affinity Reagents with Central Nervous System α-Bungarotoxin-Binding Entities. RONALD J. ... Interaction of Nicotinic Receptor Affinity Reagents with Central Nervous System α-Bungarotoxin-Binding Entities. RONALD J. ... Interaction of Nicotinic Receptor Affinity Reagents with Central Nervous System α-Bungarotoxin-Binding Entities. RONALD J. ...
Effects of Eserine and Neostigmine on the Interaction of α-Bungarotoxin with Aplysia Acetylcholine Receptors. DAVID O. ... Effects of Eserine and Neostigmine on the Interaction of α-Bungarotoxin with Aplysia Acetylcholine Receptors. DAVID O. ... Effects of Eserine and Neostigmine on the Interaction of α-Bungarotoxin with Aplysia Acetylcholine Receptors. DAVID O. ... Binding of [125I]α-bungarotoxin to acetylcholine receptors of ganglionic homogenate of the marine mollusc Aplysia is blocked by ...
sup>125I]α-bungarotoxin ligand page. Quantitative data and detailed annnotation of the targets of licensed and ...
Recombinant Protein and Acidic phospholipase A2 beta-bungarotoxin Antibody at MyBioSource. Custom ELISA Kit, Recombinant ... Shop Acidic phospholipase A2 beta-bungarotoxin ELISA Kit, ... Acidic phospholipase A2 beta-bungarotoxin Beta bungarotoxin is ... Acidic phospholipase A2 beta-bungarotoxin A chain. Acidic phospholipase A2 beta-bungarotoxin A chain ELISA Kit. Acidic ... Acidic phospholipase A2 beta-bungarotoxin A3 chain. Acidic phospholipase A2 beta-bungarotoxin A3 chain ELISA Kit. Acidic ...
... and then were tested with either a-bungarotoxin or methyllycaconitine, which are selective antagonists for nicotinic ... in which the primary postsynaptic receptors are a-bungarotoxin-sensitive nicotinic acetylcholine receptors. ... Exogenous application of acetylcholine elicits inward currents in hippocampal interneurons that are mediated via a-bungarotoxin ... Frazier, C. J., Buhler, A. V., Weiner, J. L., & Dunwiddie, T. V. (1998). Synaptic potentials mediated via alpha -bungarotoxin- ...
In GFP+ Kenyon cells, fast EPSCs are mediated by alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors (nAChRs). The ... The vast majority of spontaneous synaptic currents in the cultured Kenyon cells are mediated byalpha-bungarotoxin-sensitive ... In GFP+ Kenyon cells, fast EPSCs are mediated by alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors (nAChRs). The ... The vast majority of spontaneous synaptic currents in the cultured Kenyon cells are mediated byalpha-bungarotoxin-sensitive ...
α-bungarotoxin is a snake venom neurotoxin that acts as an antagonist at nicotinic acetylcholine receptors (nAChRs). ... "α-bungarotoxin, labeled with 125I on tyrosine residue 54. ... α-bungarotoxin is a snake venom neurotoxin that acts as an ... α-bungarotoxin, labeled with 125I on tyrosine residue 54. ... of a chimeric acetylcholine-binding protein with α-bungarotoxin ...
sup>3H]α-bungarotoxin ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental ...
When compared in nAChR-binding studies, MLA was found to compete for 125I-α-bungarotoxin binding sites (i.e. α7 sub-types) over ... Subsequently, Macallan and his co-workers showed that MLA also competed with 125I-α-bungarotoxin (Ki ~1 x 10−9M) and tritiated ... These workers also reported that MLA displaced125I-α-bungarotoxin from purified Torpedo (electric ray) nicotinic acetylcholine ... but its affinity for 125I-α-bungarotoxin binding sites is over 200x lower than that of MLA. If the -NH2 group of ...
... known as α-bungarotoxins and β-bungarotoxins, among others). By weight, almost half of the protein content of the venom is ... α-Bungarotoxin is important for neuromuscular histology, it is known to bind irreversibly to receptors of the neuromuscular ... composed of β-bungarotoxins. The average venom yield from specimens kept on snake farms is about 4.6 mg-19.4 mg per bite. The ...
α-bungarotoxin is a snake venom neurotoxin that acts as an antagonist at nicotinic acetylcholine receptors (nAChRs). ... "α-bungarotoxin, labeled with 125I on tyrosine residue 54. ... α-bungarotoxin is a snake venom neurotoxin that acts as an ... α-bungarotoxin, labeled with 125I on tyrosine residue 54. ... of a chimeric acetylcholine-binding protein with α-bungarotoxin ...
Buy alpha-bungarotoxin - an affordable,alpha7 substype selective nAChR antagonist from Hello Bio, a trusted supplier for life ... References for α-Bungarotoxin. *. Snake neurotoxin α-bungarotoxin is an antagonist at native GABA(A) receptors.. Hannan et al ( ... Inter-residue coupling contributes to high-affinity subtype-selective binding of α-bungarotoxin to nicotinic receptors.. Sine ... Neuronal acetylcholine receptors that bind alpha-bungarotoxin with high affinity function as ligand-gated ion channels.. Zhang ...
For example α-bungarotoxin is specific for nAChRs found in the musculature and κ-bungarotoxin is specific for nAChRs found in ... α-bungarotoxin, which is isolated from the banded krait snake.[39] Though extremely toxic if ingested, α-bungarotoxin has shown ... As there are multiple forms of bungarotoxin, there are different forms of nAChRs to which they will bind, and α-bungarotoxin is ... Bungarotoxin is a compound with known interaction with nicotinic acetylcholine receptors (nAChRs), which constitute a family of ...
  • Nudicauline and elatine as potent norditerpenoid ligands at rat neuronal alpha-bungarotoxin binding sites: importance of the 2-(methylsuccinimido)benzoyl moiety for neuronal nicotinic acetylcholine receptor binding. (ox.ac.uk)
  • Methyllycaconitine (MLA, 1) is a novel, potent probe for mammalian and insect nicotinic acetylcholine receptors (nAChR) and displays remarkable selectivity toward neuronal [125I]-alpha-bungarotoxin (alpha BgTX) binding sites that correspond to alpha 7-type nAChR in mammalian brain. (ox.ac.uk)
  • We have previously reported that a diet supplemented with choline induces an increase in the concentration of a brain nicotinic-like receptor, as measured by α-bungarotoxin (BuTX) binding. (nebraska.edu)
  • Morley, BJ & Garner, LL 1986, ' Increases in the concentration of brain α-bungarotoxin binding sites induced by dietary choline are age-dependent ', Brain Research , vol. 378, no. 2, pp. 315-319. (nebraska.edu)
  • Embryonic somatic nerve destruction with beta-bungarotoxin. (biomedsearch.com)
  • The effects and time course of a single injection of beta-bungarotoxin into E14 rat embryos were examined with an electron-microscopic study of development of the internal intercostal somatic nerve. (biomedsearch.com)
  • beta-Bungarotoxin applied on E17 destroyed developing axons in a similar manner, but the perineurium remained in place, and axons regenerated within the original nerve trunk. (biomedsearch.com)
  • Beta bungarotoxin is a presynaptic neurotoxin. (mybiosource.com)
  • Below are the list of possible Acidic phospholipase A2 beta-bungarotoxin products. (mybiosource.com)
  • Bungarotoxins inhibit acetylcholine binding to nicotinic acetylcholine receptors, preventing depolarisation at the postsynaptic membrane of the neuromuscular junction. (thefreedictionary.com)
  • Labeled α-bungarotoxin conjugates can be used for staining nicotinic acetylcholine receptors at neuromuscular junctions in tissue sections. (biotium.com)
  • We conclude that there are essentially no presynaptic acetylcholine receptors that bind alpha-bungarotoxin at vertebrate neuromuscular junctions. (jneurosci.org)
  • In the vertebrate brain, two categories of nicotinic receptors are distinguishable based on high-affinity binding of the agonist nicotine or high-affinity binding of the antagonist α-bungarotoxin (α-BGT). (jneurosci.org)
  • Membrane-bound α-bungarotoxin-binding entities derived from rat brain are found to interact specifically with the affinity reagents maleimidobenzyltrimethylammonium (MBTA) and bromoacetylcholine (BAC), originally designed to label nicotinic acetylcholine receptors from electroplax and skeletal muscle. (aspetjournals.org)
  • The results provide further evidence that central nervous system α-bungarotoxin receptors share a remarkable number of biochemical properties with nicotinic receptors from the periphery. (aspetjournals.org)
  • Binding of [ 125 I]α-bungarotoxin to acetylcholine receptors of ganglionic homogenate of the marine mollusc Aplysia is blocked by the anticholinesterases eserine ( I 50 = 4 µM) and neostigmine ( I 50 = 0.2 mM). (aspetjournals.org)
  • Exogenous application of acetylcholine elicits inward currents in hippocampal interneurons that are mediated via a-bungarotoxin-sensitive nicotinic acetylcholine receptors, but synaptic responses mediated via such receptors have never been reported in mammalian brain. (pacificu.edu)
  • Nicotinic EPSCs were isolated pharmacologically, using antagonists to block other known types of ligand-gated ion channels, and then were tested with either a-bungarotoxin or methyllycaconitine, which are selective antagonists for nicotinic acetylcholine receptors that contain the a7 receptor subunit. (pacificu.edu)
  • These studies provide the first demonstration of a functional cholinergic synapse in the mammalian brain, in which the primary postsynaptic receptors are a-bungarotoxin-sensitive nicotinic acetylcholine receptors. (pacificu.edu)
  • Fast synaptic currents in Drosophila mushroom body Kenyon cells are mediated by alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors and picrotoxin-sensitive GABA receptors. (escholarship.org)
  • In GFP+ Kenyon cells, fast EPSCs are mediated by alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors (nAChRs). (escholarship.org)
  • The vast majority of spontaneous synaptic currents in the cultured Kenyon cells are mediated byalpha-bungarotoxin-sensitive nAChRs or picrotoxin-sensitive GABA receptors. (escholarship.org)
  • α-bungarotoxin is a snake venom neurotoxin that acts as an antagonist at nicotinic acetylcholine receptors (nAChRs). (perkinelmer.com)
  • Snake neurotoxin α-bungarotoxin is an antagonist at native GABA(A) receptors. (hellobio.com)
  • Inter-residue coupling contributes to high-affinity subtype-selective binding of α-bungarotoxin to nicotinic receptors. (hellobio.com)
  • Neuronal acetylcholine receptors that bind alpha-bungarotoxin with high affinity function as ligand-gated ion channels. (hellobio.com)
  • Activity α-Bungarotoxin blocks postsynaptic neuromuscular transmission via competitive inhibition of nicotinic ACh receptors (nAChRs), thereby preventing the depolarizing action on postsynaptic membranes and blocking neuromuscular transmission. (alomone.com)
  • Alomone Labs α-Bungarotoxin-ATTO-633 inhibits muscle nACh receptors heterologously expressed in Xenopus oocytes. (alomone.com)
  • Methyllycaconitine (MLA, 1) is a novel, potent probe for mammalian and insect nicotinic acetylcholine receptors (nAChR) and displays remarkable selectivity toward neuronal [125I]-alpha-bungarotoxin (alpha BgTX) binding sites that correspond to alpha 7-type nAChR in mammalian brain. (ox.ac.uk)
  • Neuroprotective effect of nicotine against kainic acid excitotoxicity is associated with alpha-bungarotoxin insensitive receptors subtype of nAChRs. (nel.edu)
  • Riljak V, Benes J, Pokorný J, Myslivecek J. Neuroprotective effect of nicotine against kainic acid excitotoxicity is associated with alpha-bungarotoxin insensitive receptors subtype of nAChRs. (nel.edu)
  • Acetylcholine receptors were counterstained with fluorescent bungarotoxin (pseudocoloured blue). (biologists.org)
  • α-Bungarotoxin, a 74-amino acid peptide extracted from Bungarus multicinctus venom, binds with high affinity to the α-subunit of the nicotinic acetylcholine receptor (AChR) of neuromuscular junctions. (thermofisher.com)
  • The cDNA encoding the A chain of Β -bungarotoxin ( Β -Bgt) was constructed from the cellular RNA isolated from the venom glands of Bungarus multicinctus (Taiwan banded krait). (springer.com)
  • Extracted from Bungarus multicinctus venom, α-bungarotoxin binds with high affinity to the α-subunit of the nAChR of neuromuscular junctions. (thermofisher.com)
  • Chemical properties and amino acid composition of .BETA.1-bungarotoxin from the venom of Bungarus multicinctus (formosan banded krait). (nii.ac.jp)
  • Amino acid sequences of the two polypeptide chains in .BETA.1-bungarotoxin from the venom of Bungarus multicinctus. (nii.ac.jp)
  • bungarotoxins (.BETA.3-,.BETA.4-, and .BETA.5-bungarotoxins) from Bungarus multicinctus venom. (nii.ac.jp)
  • Amino acid sequence of .BETA.2-bungarotoxin from Bungarus multicinctus venom. (nii.ac.jp)
  • In our study, evidence is provided that strychnine, a competitive antagonist at glycine-gated Cl − channels, is also a potent competitive antagonist at native α-7-containing, α-bungarotoxin-sensitive nicotinic acetylcholine receptor (nAChRs). (aspetjournals.org)
  • We provide an extensive selection of fluorescent α-bungarotoxin conjugates ( Labeled and unlabeled alpha-bungarotoxins-Table 16.4 ) to facilitate visualization of nAChRs with a variety of instrumentation. (thermofisher.com)
  • The regulation of α-bungarotoxin-resistant nAChRs was studied on dissociated adult dorsal unpaired median neurons isolated from the terminal abdominal ganglion of the cockroach Periplaneta americana, using whole-cell, patch-clamp technique. (elsevier.com)
  • This indicated that two types of α-bungarotoxin-resistant nAChRs (named nAChR1 and nAChR2) mediated the nicotinic response. (elsevier.com)
  • We have re- examined this issue by electron microscope autoradiography with [125I] alpha-bungarotoxin, following separation of nerve terminals from muscle fibers by collagenase and protease treatment. (jneurosci.org)
  • 125I]alpha-Bungarotoxin was applied to hatchetfish medullae and a standard autoradiographic procedure was carried out on 3- to 4-microns sections of glutaraldehyde-fixed tissue. (mblwhoilibrary.org)
  • Fluorescent α-bungarotoxin conjugates can be used to facilitate identification of nicotinic AChRs and to localize neuromuscular junctions. (thermofisher.com)
  • Nicotinic AChR labeled with biotin-XX-α-bungarotoxin can be localized using enzyme or fluorophore-labeled conjugates of avidin or streptavidin (2,3). (biotium.com)
  • Conjugates of α-Bungarotoxin labeled with a selection of our CF® dyes and other labels. (biotium.com)
  • Our two longest-wavelength conjugates-Alexa Fluor 647 α-bungarotoxin ( B35450 ) and Alexa Fluor 680 α-bungarotoxin ( B35452 )-are spectrally separated from both green-fluorescent and orange-fluorescent dyes, allowing researchers to easily perform three- and four-color experiments. (thermofisher.com)
  • α-Bungarotoxin is a 74-amino acid (~8000 dalton) peptide containing 5 lysine residues and 10 cysteine residues paired in 5 disulfide bridges. (thermofisher.com)
  • METHODS: We have prepared a multivalent reactive N-(2-hydroxypropyl)methacrylamide-based copolymer (PHPMA) bearing an α-bungarotoxin-binding peptide (BTXbp). (ox.ac.uk)
  • Our bright and photostable Alexa Fluor® 647 α-bungarotoxin may prove to be one of the best probes for visualizing this receptor. (thermofisher.com)
  • Alexa Fluor 488 α-bungarotoxin ( B13422 ) has fluorescence spectra similar to those of fluorescein α-bungarotoxin ( F1176 ) and is therefore suitable for use with standard fluorescein optical filter sets. (thermofisher.com)
  • We not only offer the red-orange-fluorescent Alexa Fluor 555 α-bungarotoxin ( B35451 ), but also the red-fluorescent Alexa Fluor 594 α-bungarotoxin ( B13423 ), which has a longer-wavelength emission maximum and therefore offers better spectral separation from green-fluorescent dyes in multicolor experiments. (thermofisher.com)
  • Identification of regions involved in the binding of alpha-bungarotoxin to the human alpha7 neuronal nicotinic acetylcholine receptor using synthetic peptides. (hellobio.com)
  • The α-bungarotoxin (BGT) binding protein from rat brain has been purified and its polypeptide chain composition has been examined by sodium dodecyl sulfate polyacrylamide gel electrophoresis. (nebraska.edu)
  • We have previously reported that a diet supplemented with choline induces an increase in the concentration of a brain nicotinic-like receptor, as measured by α-bungarotoxin (BuTX) binding. (nebraska.edu)
  • Morley, BJ & Garner, LL 1986, ' Increases in the concentration of brain α-bungarotoxin binding sites induced by dietary choline are age-dependent ', Brain Research , vol. 378, no. 2, pp. 315-319. (nebraska.edu)
  • alpha-Bungarotoxin labeling and acetylcholinesterase localization at the Mauthner fiber giant synapse in the hatchetfish. (mblwhoilibrary.org)
  • Measurement of number of AChRs per EP with 125 I-labeled α-bungarotoxin and localization of AChR and acetylcholinesterase at the EP were by described methods ( 8 ). (pnas.org)
  • Under 0.5 μM α-bungarotoxin treatment, pressure ejection application of nicotine or acetylcholine onto the cell body induced an inward current exhibiting a biphasic current-voltage relationship. (elsevier.com)
  • Antibodies to alpha-bungarotoxin may sometimes be found in patients treated with snake venom. (labcorp.com)
  • Biotinylated α-bungarotoxin is useful in the affinity column isolation of the nicotinic AChR using an avidin or streptavidin agarose (1). (biotium.com)
  • Neuromuscular junctions (NMJs) were identified with α-bungarotoxin. (arvojournals.org)
  • We also offer unlabeled α-bungarotoxin and CF® Dye α-Bungarotoxin conjugated to our next-generation fluorescent dyes. (biotium.com)
  • The dynamic of Trp residue in Β 1 -bungarotoxin ( gb 1 -Bgt), the A chain of Β 1 -Bgt and phospholipase A 2 (PLA 2 ) was assessed by fluorescence measurement. (springer.com)
  • Proceedings: the effects of some bungarotoxins on skeletal muscle fibres in tissue culture. (strath.ac.uk)
  • The extent of labeling is 1-3 molecules of dye per molecule α-Bungarotoxin. (alomone.com)
  • We attach approximately one fluorophore to each molecule of α-bungarotoxin, thus retaining optimal binding specificity. (thermofisher.com)
  • The α-bungarotoxin protein (BTX) has a nanomolar binding affinity for BTXbp, allowing non-covalent linkage of BTX fusion proteins. (ox.ac.uk)
  • Paulo, J.A., Hawrot, E. (2009), Effect of homologous serotonin receptor loop substitutions on the heterologous expression in Pichia of a chimeric acetylcholine-binding protein with α-bungarotoxin-binding activity, Protein Expression and Purification, Volume 67, Issue 2, Pages 76-81. (perkinelmer.com)
  • α-bungarotoxin, labeled with 125 I on tyrosine residue 54. (perkinelmer.com)
  • Nudicauline and elatine as potent norditerpenoid ligands at rat neuronal alpha-bungarotoxin binding sites: importance of the 2-(methylsuccinimido)benzoyl moiety for neuronal nicotinic acetylcholine receptor binding. (ox.ac.uk)
  • Peroxidase-labeled α-bungarotoxin was used for the electron microscopy (EM) localization of AChR ( 9 ). (pnas.org)
  • The region of the structure containing the triple-stranded beta-sheet was, however, well defined and similar to that found in the structure of homologous alpha-bungarotoxin (45% amino acid identity). (rcsb.org)
  • An approach was therefore adopted which produced model structures based to varying degrees on the alpha-bungarotoxin structure. (rcsb.org)
  • The channel is blocked by alpha-bungarotoxin. (abcam.com)
  • See our complete selection of α-Bungarotoxin Products below. (biotium.com)
  • These results indicate that eserine and neostigmine block the binding of α-bungarotoxin by interacting with a site which is different from both the esterase and the cholinergic sites of the acetylcholine receptor. (aspetjournals.org)