Cobra Neurotoxin Proteins
Cobra Venoms
Cobra Cardiotoxin Proteins
Most abundant proteins in COBRA venom; basic polypeptides of 57 to 62 amino acids with four disulfide bonds and a molecular weight of less than 7000; causes skeletal and cardiac muscle contraction, interferes with neuromuscular and ganglionic transmission, depolarizes nerve, muscle and blood cell membranes, thus causing hemolysis.
Elapidae
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)
Neurotoxins
Eosinophil-Derived Neurotoxin
Botulinum Toxins, Type A
Clostridium botulinum
A species of anaerobic, gram-positive, rod-shaped bacteria in the family Clostridiaceae that produces proteins with characteristic neurotoxicity. It is the etiologic agent of BOTULISM in humans, wild fowl, HORSES; and CATTLE. Seven subtypes (sometimes called antigenic types, or strains) exist, each producing a different botulinum toxin (BOTULINUM TOXINS). The organism and its spores are widely distributed in nature.
Botulism
A disease caused by potent protein NEUROTOXINS produced by CLOSTRIDIUM BOTULINUM which interfere with the presynaptic release of ACETYLCHOLINE at the NEUROMUSCULAR JUNCTION. Clinical features include abdominal pain, vomiting, acute PARALYSIS (including respiratory paralysis), blurred vision, and DIPLOPIA. Botulism may be classified into several subtypes (e.g., food-borne, infant, wound, and others). (From Adams et al., Principles of Neurology, 6th ed, p1208)
Snake Venoms
Mythology
Ascorbic Acid
A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.
Diphtheria Toxin
An ADP-ribosylating polypeptide produced by CORYNEBACTERIUM DIPHTHERIAE that causes the signs and symptoms of DIPHTHERIA. It can be broken into two unequal domains: the smaller, catalytic A domain is the lethal moiety and contains MONO(ADP-RIBOSE) TRANSFERASES which transfers ADP RIBOSE to PEPTIDE ELONGATION FACTOR 2 thereby inhibiting protein synthesis; and the larger B domain that is needed for entry into cells.
Diphtheria
A localized infection of mucous membranes or skin caused by toxigenic strains of CORYNEBACTERIUM DIPHTHERIAE. It is characterized by the presence of a pseudomembrane at the site of infection. DIPHTHERIA TOXIN, produced by C. diphtheriae, can cause myocarditis, polyneuritis, and other systemic toxic effects.
NMR spatial structure of alpha-conotoxin ImI reveals a common scaffold in snail and snake toxins recognizing neuronal nicotinic acetylcholine receptors. (1/95)
A 600 MHz NMR study of alpha-conotoxin ImI from Conus imperialis, targeting the alpha7 neuronal nicotinic acetylcholine receptor (nAChR), is presented. ImI backbone spatial structure is well defined basing on the NOEs, spin-spin coupling constants, and amide protons hydrogen-deuterium exchange data: rmsd of the backbone atom coordinates at the 2-12 region is 0.28 A in the 20 best structures. The structure is described as a type I beta-turn (positions 2-5) followed by a distorted helix (positions 5-11). Similar structural patterns can be found in all neuronal-specific alpha-conotoxins. Highly mobile side chains of the Asp-5, Arg-7 and Trp-10 residues form a single site for ImI binding to the alpha7 receptor. When depicted with opposite directions of the polypeptide chains, the ImI helix and the tip of the central loop of long chain snake neurotoxins demonstrate a common scaffold and similar positioning of the functional side chains, both of these structural elements appearing essential for binding to the neuronal nAChRs. (+info)Subunit interface selectivity of the alpha-neurotoxins for the nicotinic acetylcholine receptor. (2/95)
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)Snake venom alpha-neurotoxins and other 'three-finger' proteins. (3/95)
The review is mainly devoted to snake venom alpha-neurotoxins which target different muscle-type and neuronal nicotinic acetylcholine receptors. The primary and spatial structures of other snake venom proteins as well as mammalian proteins of the Ly-6 family, which structurally resemble the 'three-finger' snake proteins, are also briefly discussed. The main emphasis is placed on recent data characterizing the alpha-neurotoxin interactions with nicotinic acetylcholine receptors. (+info)How do acetylcholine receptor ligands reach their binding sites? (4/95)
The access pathway to the binding sites for large competitive antagonists of the nicotinic acetylcholine receptor from Torpedo californica electric tissue was analyzed by binding and photolabeling experiments with alpha-neurotoxins. Binding assays with [125I]alpha-bungarotoxin showed an increase in the number of accessible binding sites upon stepwise solubilization of the receptor-rich membranes. Similarily, ligand binding is facilitated upon fluidization of the membrane by increasing the temperature. The access to the binding sites seems to be sterically 'hindered' in the densely packed membrane state. Using a novel series of large biotinylated photoactivatable derivatives of neurotoxin II, we observed that the accessibility to the alpha/gamma- but not to the alpha/delta-binding site was considerably decreased for some derivatives under native conditions. This effect was less apparent at higher temperatures and could be abolished by complete solubilization. These observations support the nonequivalence of the receptor's binding sites. Together, our data suggest (a) that alpha-neurotoxins approach their binding sites from the membrane-facing periphery of the receptor's extramembrane domain rather than through the channel mouth and (b) that different entrance pathways to each binding site exist which vary in their sensitivity to the physical state of the plasma membrane. (+info)Variability among the sites by which curaremimetic toxins bind to torpedo acetylcholine receptor, as revealed by identification of the functional residues of alpha-cobratoxin. (5/95)
alpha-Cobratoxin, a long chain curaremimetic toxin from Naja kaouthia venom, was produced recombinantly (ralpha-Cbtx) from Escherichia coli. It was indistinguishable from the snake toxin. Mutations at 8 of the 29 explored toxin positions resulted in affinity decreases for Torpedo receptor with DeltaDeltaG higher than 1.1 kcal/mol. These are R33E > K49E > D27R > K23E > F29A >/= W25A > R36A >/= F65A. These positions cover a homogeneous surface of approximately 880 A(2) and mostly belong to the second toxin loop, except Lys-49 and Phe-65 which are, respectively, on the third loop and C-terminal tail. The mutations K23E and K49E, and perhaps R33E, induced discriminative interactions at the two toxin-binding sites. When compared with the short toxin erabutoxin a (Ea), a number of structurally equivalent residues are commonly implicated in binding to muscular-type nicotinic acetylcholine receptor. These are Lys-23/Lys-27, Asp-27/Asp-31, Arg-33/Arg-33, Lys-49/Lys-47, and to a lesser and variable extent Trp-25/Trp-29 and Phe-29/Phe-32. In addition, however, the short and long toxins display three major differences. First, Asp-38 is important in Ea in contrast to the homologous Glu-38 in alpha-Cbtx. Second, all of the first loop is insensitive to mutation in alpha-Cbtx, whereas its tip is functionally critical in Ea. Third, the C-terminal tail may be specifically critical in alpha-Cbtx. Therefore, the functional sites of long and short curaremimetic toxins are not identical, but they share common features and marked differences that might reflect an evolutionary pressure associated with a great diversity of prey receptors. (+info)Molecular determinants by which a long chain toxin from snake venom interacts with the neuronal alpha 7-nicotinic acetylcholine receptor. (6/95)
Long chain curarimimetic toxins from snake venom bind with high affinities to both muscular type nicotinic acetylcholine receptors (AChRs) (K(d) in the pm range) and neuronal alpha 7-AChRs (K(d) in the nm range). To understand the molecular basis of this dual function, we submitted alpha-cobratoxin (alpha-Cbtx), a typical long chain curarimimetic toxin, to an extensive mutational analysis. By exploring 36 toxin mutants, we found that Trp-25, Asp-27, Phe-29, Arg-33, Arg-36, and Phe-65 are involved in binding to both neuronal and Torpedo (Antil, S., Servent, D., and Menez, A. (1999) J. Biol. Chem. 274, 34851-34858) AChRs and that some of them (Trp-25, Asp-27, and Arg-33) have similar binding energy contributions for the two receptors. In contrast, Ala-28, Lys-35, and Cys-26-Cys-30 selectively bind to the alpha 7-AChR, whereas Lys-23 and Lys-49 bind solely to the Torpedo AChR. Therefore, alpha-Cbtx binds to two AChR subtypes using both common and specific residues. Double mutant cycle analyses suggested that Arg-33 in alpha-Cbtx is close to Tyr-187 and Pro-193 in the alpha 7 receptor. Since Arg-33 of another curarimimetic toxin is close to the homologous alpha Tyr-190 of the muscular receptor (Ackermann, E. J., Ang, E. T. H., Kanter, J. R., Tsigelny, I., and Taylor, P. (1998) J. Biol. Chem. 273, 10958-10964), toxin binding probably occurs in homologous regions of neuronal and muscular AChRs. However, no coupling was seen between alpha-Cbtx Arg-33 and alpha 7 receptor Trp-54, Leu-118, and Asp-163, in contrast to what was observed in a homologous situation involving another toxin and a muscular receptor (Osaka, H., Malany, S., Molles, B. E., Sine, S. M., and Taylor, P. (2000) J. Biol. Chem. 275, 5478-5484). Therefore, although occurring in homologous regions, the detailed modes of toxin binding to alpha 7 and muscular receptors are likely to be different. These data offer a molecular basis for the design of toxins with predetermined specificities for various members of the AChR family. (+info)Binding properties of agonists and antagonists to distinct allosteric states of the nicotinic acetylcholine receptor are incompatible with a concerted model. (7/95)
Recent work has shown that the nicotinic acetylcholine receptor (nAChR) can be fixed in distinct conformations by chemical cross-linking with glutardialdehyde, which abolishes allosteric transitions in the protein. Here, two conformations that resemble the desensitized and the resting states were compared with respect to their affinities for different classes of ligands. The same ligands were tested for their ability to convert the nAChR from a conformation with low affinity to a conformation with high affinity for acetylcholine. As expected, agonists were found to bind with higher affinity to the desensitized state-like conformation and to induce a shift of the nAChR to this high affinity state. In contrast, although most antagonists tested bound preferentially to the desensitized receptor as well they failed to induce a change of the affinity for acetylcholine. These observations sharply contradict basic predictions of the concerted model, including the postulate of a preformed equilibrium between the different states of the nAChR in the absence of agonist. With a similar approach we could show that the non-competitive inhibitor ethidium is displaced in a non-allosteric manner by other well characterized channel blockers from the cross-linked nAChR. These results require revision of current models for the mechanisms underlying non-competitive antagonism at the nAChR. (+info)"Weak toxin" from Naja kaouthia is a nontoxic antagonist of alpha 7 and muscle-type nicotinic acetylcholine receptors. (8/95)
A novel "weak toxin" (WTX) from Naja kaouthia snake venom competes with [(125)I]alpha-bungarotoxin for binding to the membrane-bound Torpedo californica acetylcholine receptor (AChR), with an IC(50) of approximately 2.2 microm. In this respect, it is approximately 300 times less potent than neurotoxin II from Naja oxiana and alpha-cobratoxin from N. kaouthia, representing short-type and long-type alpha-neurotoxins, respectively. WTX and alpha-cobratoxin displaced [(125)I]alpha-bungarotoxin from the Escherichia coli-expressed fusion protein containing the rat alpha7 AChR N-terminal domain 1-208 preceded by glutathione S-transferase with IC(50) values of 4.3 and 9.1 microm, respectively, whereas for neurotoxin II the IC(50) value was >100 microm. Micromolar concentrations of WTX inhibited acetylcholine-activated currents in Xenopus oocyte-expressed rat muscle AChR and human and rat alpha7 AChRs, inhibiting the latter most efficiently (IC(50) of approximately 8.3 microm). Thus, a virtually nontoxic "three-fingered" protein WTX, although differing from alpha-neurotoxins by an additional disulfide in the N-terminal loop, can be classified as a weak alpha-neurotoxin. It differs from the short chain alpha-neurotoxins, which potently block the muscle-type but not the alpha7 AChRs, and is closer to the long alpha-neurotoxins, which have comparable potency against the above-mentioned AChR types. (+info)
Identification and isolation of immunodominant proteins of Naja naja (Oxiana) snake venom
RCSB PDB
- 1LXG: Solution structure of alpha-cobratoxin complexed with a cognate peptide (structure ensemble)...
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Toxins | Free Full-Text | Interactions of PLA2-s from Vipera lebetina, Vipera berus berus and Naja naja oxiana Venom with...
Cobra venom molecule - Stock Image F006/9278 - Science Photo Library
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Structure Cluster
- 1COD: SOLUTION CONFORMATION OF COBROTOXIN: A NUCLEAR MAGNETIC RESONANCE AND HYBRID DISTANCE...
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Depolarization of skeletal muscle cells in culture by a cardiotoxin-like basic polypeptide from the venom of the Taiwan cobra ...
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Purification of a post-synaptic neurotoxic phospholipase A2 from Naja naja venom and its inhibition by a glycoprotein from...
It is denoted to be a basic protein by its behavior on both ion exchange chromatography and electro … ... has been purified from Indian cobra Naja naja venom. It was associated with a peptide in the venom. The association was ... Cobra Neurotoxin Proteins / antagonists & inhibitors* * Cobra Neurotoxin Proteins / isolation & purification * Dose-Response ... The WSG inhibited the phospholipase A(2) activity of NN-XIa-PLA(2,) isolated from the cobra venom, completely at a mole-to-mole ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DoctorYourself.com - Klenner Vitamin C Paper
Neurotoxin from the Black Widow, the Fiddle Spider and snakes like the Cobra and Coral; ... The infectious nucleic acid, after entering a human cell, retains its protein coat and starts to produce its own type protein ... Formic acid plus a toxin with a protein cover, called proteotoxin by Arthus,[39] such as found in bees and wasps; ... The role of the protein coat is to protect the parasitic but unstable nucleic acid as it rides the "blood highway" or " ...
Reptiles And Amphibians In Pharmaceutical Research - Reptiles Magazine
The king cobra (Ophiophagus hannah) possesses a unique protein called ohanin, which is made up of only 107 amino acids. By ... Cobra venoms consist primarily of neurotoxins and are fast acting, quickly crippling the nervous system, which results in ... The king cobra (Ophiophagus hannah) possesses a unique protein called ohanin, which is made up of only 107 amino acids. ... The venoms of more than 100 C. rhodostoma were analyzed; in all populations, females produced an intense protein band that was ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
DeCS 2008 - Changed terms
Cobra Neurotoxins. Cobra Neurotoxin Proteins. Direct Lytic Factors. Cobra Cardiotoxin Proteins. D23 - Biological Factors. Shiga ... SHP1 Protein Tyrosine Phosphatase. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Thioredoxin Reductase (NADPH). ... Protein Isoprenylation. Protein Prenylation. G09 - Circulatory and Respiratory Physiology. Hemodynamic Processes. Hemodynamics ... Ca(2+)-Calmodulin Dependent Protein Kinase. Calcium-Calmodulin-Dependent Protein Kinases. Cholesterol Esterase. Sterol Esterase ...
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Ardis: Corona comes from snake poison in the drinking water - bats in Wuhan still had hibernation - genetics of King Cobra and ... proteins in the Pfizer GENE vaccines: Stew Peters Show: Dr. Jane Ruby Drops Photos Provided by Scientists: ... King Cobra - Dr. Ardis -- April 20, 2022: Lachesis against sepsis (blood poisoning) Concerning snake venoms and Lachesis -- ... Spike proteins contain peptides which are similar to peptides of neurotoxins in snake venom: King cobra and Krait (Bungarus)]. ...
Naja - Wikipedia
Short Alpha-Neurotoxins as the Dominant Lethal Component Weakly Cross-Neutralized by the Philippine Cobra Antivenom". Frontiers ... International Journal of Peptide and Protein Research. 6 (4): 201-222. doi:10.1111/j.1399-3011.1974.tb02380.x. PMID 4426734.. ... Mandalay spitting cobra (Burmese spitting cobra) Myanmar (Burma) N. melanoleuca Hallowell, 1857 0 Central African forest cobra ... Cape cobra (yellow cobra) Botswana, Lesotho, Namibia, South Africa N. nubiae Wüster & Broadley, 2003 0 Nubian spitting cobra ...
Dr. Klenner 1<...
Formic acid plus a toxin with a protein cover, called proteotoxin by Arthus,[39] such as found in bees and wasps;. · Neurotoxin ... from the Black Widow, the Fiddle Spider and snakes like the Cobra and Coral;. · Production of histamine, especially in the more ... The infectious nucleic acid, after entering a human cell, retains its protein coat and starts to produce its own type protein ... As with the virus bodies, ascorbic acid also joins with the protein factor of these toxins effecting quick destruction. ...
Antivenenos/farmacologia
The major components in the venom are cytotoxins/cardiotoxins (~75.6% of total venom proteins) and alpha-neurotoxins (~7.4%), ... In addition, the neutralizing capability of Cobra Antivenom (CAV), King Cobra Antivenom (KCAV) and Neuro Polyvalent Antivenom ( ... Previous studies characterized the protein composition of its venom, with phospholipase A2 (PLA2) proteins the most abundant. ... Cobras Corais , Toxinas Biológicas , Animais , Coelhos , Humanos , Antivenenos/farmacologia , Peru , Venenos Elapídicos/química ...
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For instance, while the venom of the West Bengal population of monocled cobra was rich in neurotoxins, the venom of the ... 3FTx is amongst the most potent neurotoxic proteins that enriches the venoms of many advanced snakes, including cobras and ... The Andaman cobra (N. sagittifera) is genetically closer to its southeast Asian counterpart (Photo courtesy: ANET) ... Thus, the discovery of these neurotoxins in ancient groups of snakes points to a single early origin of venom in this lineage. ...
Mind-Blowing: Could the Origin of COVID Be From a Symbol of Evil? - 'Watch the Water' [VIDEO]
I have believed that this "spike protein" was a neurotoxin ever since I heard Dr Carrie Maddei (sp??) talk about the man made ... King Cobra? Coral? There are only so many but each is deadly. Mamba, does it cause clots? Which one of the deadliest does? But ... The 3d structure of the spike protein looks very similar to some snake-venom proteins. Also many of the adverse events from the ... sequencing of Spike proteins, trying to solve the mystery of SARS COVID 2 victims and he says hes got a big thing to.. big ...
Cobra Venom-19? - NoFakeNews.net
Suramins ability to block P2 purinergic, G protein-coupled receptors (82) may counteract the action of neurotoxins that ... What are these 19 neurotoxins, and where do they come from? Cobra venom! As in Cobra-19! ... Ardis believes the King Cobra and Krait snakes were the venoms used because of the 19 neurotoxins they contain. ... Ardis also believes that the mRNA bioweapons create the protein structures of the synthetic snake venom and that these proteins ...
Institute of Chemistry, Academia Sinica--Ding-Kwo Chang
Yu C Proline inhibits aggregation during protein refolding.. Protein science : a publication of the Protein Society 2000, 9(2), ... Bhaskaran, R.; Huang, C.-C.; Tsai, Y.-C.; Jayaraman, G.; Chang, D.-K.; Yu, C. Cardiotoxin II from Taiwan cobra venom, Naja naja ... determination of structure in solution and comparison with short neurotoxins. J. Mol. Biol. 1994, 235, 1291. ... paper presented at 10th FAOB Symposium on Protein Research, ?: 10th FAOB Symposium on Protein Research, 1993. ...
Lpmhealthcare » Posters
Upregulation of the toxins long neurotoxin 1, long neurotoxin OH-55, short neurotoxin 2, Zn-dependent-metalloproteanase- ... The African non-spitting cobra Naja nivea (Cape cobra) is endemic to South Africa and one of the most medically significant ... In the electrophoresis gel, a 23 kDa band was observed at day 4, similar in size to the native protein BpMtx-I. In this way, ... Naja ashei (giant spitting cobra) is one of the lesser-known representatives of African spitting cobras, inhabiting open and ...
Кудрявцев Денис Сергеевич - пользователь, сотрудник | ИСТИНА - Интеллектуальная Система Тематического Исследования...
2021 Novel Three-Finger Neurotoxins from Naja melanoleuca Cobra Venom Interact with GABAA and Nicotinic Acetylcholine Receptors ... 2016 Human Secreted Ly-6/uPAR Related Protein-1 (SLURP-1) Is a Selective Allosteric Antagonist of α7 Nicotinic Acetylcholine ... 2021 Novel Three-Finger Neurotoxins from Naja melanoleuca Cobra Venom Interact with GABAA and Nicotinic Acetylcholine Receptors ... 2015 Neurotoxins from Snake Venoms and α-Conotoxin ImI Inhibit Functionally Active Ionotropic γ-Aminobutyric Acid (GABA) ...
Venomous Snakes Of India - Wildlife SOS
Composed of a variety of proteins, enzymes, anti-coagulants, neurotoxins, and other substances, snake venom is a complex ... Distributed throughout India, mostly kraits and cobras fall under this family.. *Hydrophiidae - Snakes in this family have ... They include spectacled cobra (Naja naja), common krait (Bungarus caeruleus), Russells viper (Daboia russelii), and saw-scaled ...