Disease relevance of Cobra

• Doses of lipocortin that produced approximately 50% inhibition in the carrageenin test were inactive against edema elicited by bradykinin, serotonin, platelet-activating factor-acether, or dextran, whereas edema caused by Naja mocambique venom phospholipase A2 was strongly inhibited by lipocortin [1].
• Exogenous phospholipase A2 [from Naja naja (Indian cobra) venom] and phospholipase C (from Clostridium welchii) stimulated prostaglandin E2 production in a dose-dependent manner [2].
• Effect of ranitidine bismuth citrate on the phospholipase A2 activity of Naja naja venom and Helicobacter pylori: a biochemical analysis [3].
• Acetylcholine receptors in the ciliary ganglion and in the iris muscle of the chick: specific binding and effect on the synaptic transmission of the neurotoxin from Naja naja siamensis [4].
• Hemolysis induced by halothane and the N. n. kaouthia or Naja naja atra CTXs was enhanced by unsaturated fatty acids [5].

High impact information on Cobra

• We conclude that anticholinesterases are beneficial in the management of neurotoxic envenoming by Asian cobras (Naja naja), and we recommended a test of edrophonium in any patient with signs of neurotoxic envenoming after snakebite [6].
• Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study [6].
• The first is the structure of the PLA2 from the venom of the Chinese cobra (Naja naja atra) in a complex with a phosphonate transition-state analogue [7].
• Evidence is presented that cobra venom factor, the anticomplementary protein in Naja naja venom, is modified cobra C3 (the third component of complement) [8].
• In order to block acetylcholine receptors of muscle, the alpha toxin of the Formosan cobra (Naja naja atra) was given intravenously to rats [9].

Chemical compound and disease context of Cobra

• When co-inhibited with Naja naja phospholipase A2 or histamine the peptide did not modify the swelling at doses up to 500 ng, showing at 5 micrograms an additive edema with Naja naja phospholipase A2 [10].
• The basic phospholipase A2 from Naja nigricollis snake venom is cardiotoxic, causing decreased contractility and arrhythmias at concentrations which induce low levels of phospholipid hydrolysis [11].
• Effect of calcium and phosphate ions on hemolysis induced by Pyrularia thionin and Naja naja kaouthia cardiotoxin [12].
• We report here the construction of cardiotoxin V gene, from cobra snake venom (Naja naja atra), by chemically synthesized oligonucleotides and its expression as a glutathione S-transferase-cardiotoxin fusion protein in the inclusion bodies of Escherichia coli [13].
• We report that sphingosine directly inhibits phospholipases A2 and D. Sphingosine inhibits Ca(2+)-dependent phospholipases A2 from Naja naja, porcine pancreas, Crotalus adamanteus, human disc and neutrophil in a dose-dependent manner with IC50 values ranging from 5-40 microM using [1-14C]oleate-labelled autoclaved E. coli (20 microM) as substrate [14].

Biological context of Cobra

• Perturbation of the surface phospholipid monolayer of the emulsion particle as a result of hydrolysis by Naja naja phospholipase A2 resulted in a 10-fold activation of LPL, providing further support for an interfacial penetration model [15].
• The complete amino acid sequence of a cardiotoxin from the venom of Naja naja (Cambodian Cobra) [16].
• METHODS: In this study we measured and analysed the inhibitory effect of ranitidine bismuth citrate (RBC, Pylorid, Tritec) on the activity and kinetics of phospholipase A2 (PLA2) (E.C.3.1.1.4) of commercial cobra (Naja naja) venom and H. pylori (French press lysates) using L-alpha-dipalmitoyl-(2[1-14C]palmitoyl)-phosphatidylcholine as substrate [3].
• Conformational studies of neurotoxin II from Naja naja oxiana. Selective N-acylation, circular dichroism and nuclear-magnetic-resonance study of acylation products [17].
• Ircinin inhibited Naja naja venom, human synovial recombinant, bee venom and zymosan-injected rat air pouch PLA2 with IC50 values in the microM range, similar to those of the known inhibitor scalaradial [18].

Anatomical context of Cobra

• We have studied the stoichiometry of the binding of the long alpha-neurotoxins from the venom of Dendroaspis viridis (alpha-dendrotoxin) and Naja naja siamensis (alpha-cobratoxin) to the membrane-bound acetylcholine receptor (AcChoR) from Torpedo californica electric organ [19].
• The solubilized [3H]acetylcholine binding activity is separated from the toxin receptor by incubation with agarose-linked acetylcholine, by affinity chromatography on immobilized Naja naja siamensis alpha-toxin, and by precipitation with a monoclonal antibody to chick optic lobe toxin receptor [20].
• Cardiotoxin isolated from Naja mossambica mossambica selectively deactivates the sodium-potassium activated adenosine triphosphatase of axonal membranes [21].
• In the present study, the inactivation of the phospholipases A2 from pig pancreas, bee venom, and cobra (Naja naja naja) venom by manoalogue was studied in detail [22].
• The effect of a cardiotoxic component of the venom of the indian cobra (Naja nigricollis) on the subcellular structure and function of heart muscle [23].

Associations of Cobra with chemical compounds

• A photoactivatable derivative of neurotoxin II from Naja naja oxiana containing a 125I-labeled p-azidosalicylamidoethyl-1,3'-dithiopropyl label at Lys-25 forms a photo-induced cross-link with the delta subunit of the membrane-bound Torpedo californica nicotinic acetylcholine receptor (AChR) [24].
• Phospholipase A2 (PLA2) from Indian cobra venom (Naja naja naja) was crystallized from ethanol in space group P4(3)2(1)2 in the presence of Ca2+ [25].
• Exposure of receptor-rich membrane fragments from Torpedo marmorata to carbamylcholine causes a slow (half-time of 5--10 min) and reversible change of properties of the cholinergic receptor protein manifested by a decrease of the initial rate of Naja nigricollis alpha-[3H]toxin binding in the presence of carbamylcholine [26].
• The inhibition potency obtained was alpha-bungarotoxin greater than Naja naja siamensis toxin greater than d-tubocurarine greater than decamethonium greater than acetylcholine greater than carbamoylcholine [27].
• A peptide of acetylcholinesterase (AcChoEase; acetylcholine acetylhydrolase, EC 3.1.1.7) from the venom of the cobra Naja naja oxiana labeled by the affinity reagent N,N-dimethyl-2-phenylaziridinium (DPA) has been identified [28].

Gene context of Cobra

• In comparison, sPLA2 from Naja naja venom (Group I) also showed only modest activity with this substrate [29].
• A von Willebrand factor (vWF)-binding and -cleaving metalloproteinase, termed "kaouthiagin", was purified from the venom of cobra snake Naja kaouthia [30].
• For instance, the RMSd for the backbone atoms between MTX2 and the curaremimetic toxin alpha (from Naja nigricollis), the acetylcholinesterase inhibitor fasciculin 1 (from Dendroaspis angusticeps), and the cardiotoxic toxin gamma (from Naja nigricollis) are 1.86, 1.87, and 2.04 A, respectively [31].
• Our data show that recombinant human enzyme PLA2 (0.01-10 micrograms/pouch), but not Naja mocambique mocambique (Group 2 PLA2) and porcine pancreatic PLA2 (Group 1 PLA2), was able to exacerbate the inflammatory response without increasing eicosanoid release [32].
• We have observed that a wide variety of cells in culture contain high levels of endogenous PLase that can be activated by polypeptide toxins, such as melittin purified from bee venom and direct lytic factor purified from the venom of African Ringhals cobra (Hemachatus hemachatus) [33].

Analytical, diagnostic and therapeutic context of Cobra

• Circular dichroism spectroscopy has been used to study the unfolding-refolding process of a cardiotoxin from Taiwan cobra (Naja naja atra) venom upon addition of fluoroalcohols or sodium dodecyl sulfate (SDS) to its aqueous solution [34].
• The general applicability of our immobilization protocol was demonstrated by the high retention of activity achieved for the immobilized acylated PLA2 from the venom of Naja naja naja [35].
• Interaction of modified neurotoxins from Naja nigricollis with the nicotinic acetylcholine receptor from Torpedo marmorata. A Raman spectroscopy study [36].
• Charge isoforms of cobra (Naja naja oxiana) venom acetylcholinesterase, separated by isoelectric focusing, differ only by the number of free carboxyl groups of glutamic and/or aspartic acid side-chains in the enzyme molecule [37].
• Surface plasmon resonance studies have shown that niflumic acid binds to Naja naja sagittifera PLA(2) with an affinity that corresponds to a dissociation constant (K(d)) of 4.3 x 10(-5) M [38].

References