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At least 19 recordsLinked to original sources
PubMed2026

A Pseudokinase Catalyzes Nitrile Formation in the Biosynthesis of a Potent Marine Toxin.

Several pseudokinases, previously regarded as dead enzymes due to the lack of catalytic residues, catalyze nucleotidylation. While they often utilize macromolecular substrates such as proteins and RNAs in primary metabolism, those acting on non-macromolecules in specialized metabolisms are limited. Calyculin A, a cytotoxic natural product produced by an uncultured sponge symbiont, possesses a unique nitrile group at the end of its tetraene tail. Even though its biosynthetic gene cluster (BGC) has been identified, the enzyme responsible for nitrile formation remains unknown. Herein, through a comparative analysis of the BGCs for calyculin derivatives in symbiotic bacteria from distinct sources, we identified a novel nitrile-forming enzyme, CalN. While CalN lacks sequence homology with other known nitrile-forming enzymes, it is structurally similar to pseudokinases. In vitro enzymatic reactions demonstrated that CalN specifically catalyzes nitrile formation through the adenylation of an amide substrate, calyculinamide A. In silico analyses and mutational experiments showed that CalN's structure features a unique insertion that plays critical roles in ATP recognition and the spatial coordination of catalytic residues. This study not only identifies a new family of nitrile-forming enzymes but also expands the variety of chemical reactions mediated by pseudokinases in nature.

Marine Toxins↗
PubMed1975

The neurologic effects of noxious marine creatures.

The concept of the sea as a source of noxious agents is perhaps not a familiar one to clinical neurologists, judging by the lack of reference to these agents in standard textbooks. Chemical, physiologic, and pharmacologic laboratories are increasingly investigating the properties of marine toxins, finding in them compounds with interesting and novel structures or unusual physiologic effects. Such substances are seen as possible agents for biologic and, more particularly, physiologic research, and as possible sources of new pharmaceuticals. These include hormone-like substances and antiviral or antitumor agents. Despite these specialized developments, which are in large measure a consequence of the technological advances of the present century, the clinician is at times directly concerned with the effects of marine toxic substances. For example, in Japan, puffer fish or tetrodotoxic poisoning is one of the major causes of deaths from food poisoning. Another marine toxin that has caused many explosive outbreaks of food poisoning. with many deaths in various parts of the world, comes from clams or mussels. This toxin, saxitoxin, is produced by species of marine protozoa including Gonyaulax, and is concentrated in filter-feeding molluscs. These two examples were of significant interest in medicine long before the technologic developments of the twentieth century. In the last few decades, entirely new problems of marine intoxication have arisen as a result of marine pollution from the disposal of industrial wastes in the sea. The most striking example of a man-made marine intoxication has been the outbreak of Minamata disease. In Minamata, Japan, the disposal of mercury-contaminated industrial wastes from a plastics factory into an enclosed bay, followed by human consumption of the contaminated fishes, crabs, or shellfish, led to many instances of acute cerebral degeneration. With the increasing exploration of the sea for both pleasure and economic exploitation, which is a feature of the second half of the twentieth century, it may be expected that the frequency and variety of human intoxications by marine creatures will be increased. This chapter reviews the neurologic effects of noxious substances of marine biologic origin. The subject is now developing so rapidly that overall surveys, such as this, of the general animal life of theocens will soon be beyond the scope of a single review. Nevertheless, it is hoped that the references given will enable the interested reader to pursue particular aspects further.

Adult↗
PubMedDate not supplied

Mechanism of action of neurotoxins.

This paper is a summary of studies over the past few years that pertain to animal neurotoxins. These toxins are found throughout the animal kingdom. Homologies exist in the structures of these poisons within classes and point to conservation of active sites throughout evolution. In the case of the peptides, invariant amino acids may be involved in the active site, be essential for maintaining the shape and conformation of the molecule or serve as a fulcrum for folding of the peptide chain after synthesis. At the nuclear or DNA-level, a constant base sequence may regulate gene operation so that only a specific amino acid is coded. Physiologically, and with ultrastructural and biochemical correlation, the predominant mode of action of neurotoxins relate to one or the other of the major activities of the excitable cell,--on conductile activity affecting Na+ or K+ permeabilities, on output or secretory activities affecting the release of neurotransmitter or on in put generator activities affecting the receptor molecules for transmitter themselves. The future of these animal neurotoxins in neurobiological research is secure. The elucidation of molecular mechanisms, by which these various physiological activities of excitable tissue are expressed, will surely involve one or more of these fascinating, naturally-occurring compounds.

Animals↗
PubMed1978

Dermatitis from purified sea algae toxin (debromoaplysiatoxin).

Cutaneous inflammation was induced by debromoaplysiatoxin, a purified toxin extracted from Lyngbya majuscula Gomont. This alga causes a seaweed dermatitis that occurs in persons who have swum off the coast of Oahu in Hawaii. By topical application, the toxin was found to produce an irritant pustular folliculitis in humans and to cause a severe cutaneous inflammatory reaction in the rabbit and in hairless mice.

Animals↗