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• W2596099863 endingPage "107" @default.
• W2596099863 startingPage "107" @default.
• W2596099863 abstract "An understanding of the molecular mechanisms by which microbial, plant or animal-secreted toxins exert their action provides the most important element for assessment of human health risks and opens new insights into therapies addressing a plethora of pathologies, ranging from neurological disorders to cancer, using toxinomimetic agents. Recently, molecular and cellular biology dissecting tools have provided a wealth of information on the action of these diverse toxins, yet, an integrated framework to explain their selective toxicity is still lacking. In this review, specific examples of different toxins are emphasized to illustrate the fundamental mechanisms of toxicity at different biochemical, molecular and cellular- levels with particular consideration for the nervous system. The target of primary action has been highlighted and operationally classified into 13 sub-categories. Selected examples of toxins were assigned to each target category, denominated as portal, and the modulation of the different portal's signaling was featured. The first portal encompasses the plasma membrane lipid domains, which give rise to pores when challenged for example with pardaxin, a fish toxin, or is subject to degradation when enzymes of lipid metabolism such as phospholipases A₂ (PLA₂) or phospholipase C (PLC) act upon it. Several major portals consist of ion channels, pumps, transporters and ligand gated ionotropic receptors which many toxins act on, disturbing the intracellular ion homeostasis. Another group of portals consists of G-protein-coupled and tyrosine kinase receptors that, upon interaction with discrete toxins, alter second messengers towards pathological levels. Lastly, subcellular organelles such as mitochondria, nucleus, protein- and RNA-synthesis machineries, cytoskeletal networks and exocytic vesicles are also portals targeted and deregulated by other diverse group of toxins. A fundamental concept can be drawn from these seemingly different toxins with respect to the site of action and the secondary messengers and signaling cascades they trigger in the host. While the interaction with the initial portal is largely determined by the chemical nature of the toxin, once inside the cell, several ubiquitous second messengers and protein kinases/ phosphatases pathways are impaired, to attain toxicity. Therefore, toxins represent one of the most promising natural molecules for developing novel therapeutics that selectively target the major cellular portals involved in human physiology and diseases." @default.
• W2596099863 created "2017-03-23" @default.
• W2596099863 creator A5017829582 @default.
• W2596099863 creator A5049332135 @default.
• W2596099863 creator A5076958866 @default.
• W2596099863 date "2017-03-16" @default.
• W2596099863 modified "2023-10-01" @default.
• W2596099863 title "The Molecular Basis of Toxins’ Interactions with Intracellular Signaling via Discrete Portals" @default.
• W2596099863 cites W1131789609 @default.
• W2596099863 cites W129191972 @default.
• W2596099863 cites W141015732 @default.
• W2596099863 cites W1444797862 @default.
• W2596099863 cites W1480239515 @default.
• W2596099863 cites W1492287582 @default.
• W2596099863 cites W1497728911 @default.
• W2596099863 cites W1503830589 @default.
• W2596099863 cites W150678807 @default.
• W2596099863 cites W1506887116 @default.
• W2596099863 cites W1515985765 @default.
• W2596099863 cites W1520446061 @default.
• W2596099863 cites W1528142343 @default.
• W2596099863 cites W1530842205 @default.
• W2596099863 cites W1531585137 @default.
• W2596099863 cites W1531902018 @default.
• W2596099863 cites W1532284082 @default.
• W2596099863 cites W1543515175 @default.
• W2596099863 cites W1563624749 @default.
• W2596099863 cites W1568523124 @default.
• W2596099863 cites W1577883243 @default.
• W2596099863 cites W1581155900 @default.
• W2596099863 cites W1582713108 @default.
• W2596099863 cites W1591373153 @default.
• W2596099863 cites W1593385535 @default.
• W2596099863 cites W1594106664 @default.
• W2596099863 cites W1594450461 @default.
• W2596099863 cites W1602619794 @default.
• W2596099863 cites W1605435161 @default.
• W2596099863 cites W1624744767 @default.
• W2596099863 cites W1699538611 @default.
• W2596099863 cites W1735272425 @default.
• W2596099863 cites W1749352888 @default.
• W2596099863 cites W1749453950 @default.
• W2596099863 cites W1759648464 @default.
• W2596099863 cites W1776318968 @default.
• W2596099863 cites W1785056813 @default.
• W2596099863 cites W1798133325 @default.
• W2596099863 cites W1822767616 @default.
• W2596099863 cites W1842440437 @default.
• W2596099863 cites W1892434417 @default.
• W2596099863 cites W1904956466 @default.
• W2596099863 cites W1909956655 @default.
• W2596099863 cites W1910528605 @default.
• W2596099863 cites W191075349 @default.
• W2596099863 cites W1919056206 @default.
• W2596099863 cites W192621565 @default.
• W2596099863 cites W1938591788 @default.
• W2596099863 cites W1947863176 @default.
• W2596099863 cites W1948473377 @default.
• W2596099863 cites W1954540662 @default.
• W2596099863 cites W1963561206 @default.
• W2596099863 cites W1964372470 @default.
• W2596099863 cites W1964609746 @default.
• W2596099863 cites W1966118942 @default.
• W2596099863 cites W1966951820 @default.
• W2596099863 cites W1967023505 @default.
• W2596099863 cites W1967868924 @default.
• W2596099863 cites W1967924344 @default.
• W2596099863 cites W1967980896 @default.
• W2596099863 cites W1968219212 @default.
• W2596099863 cites W1969122043 @default.
• W2596099863 cites W1969192901 @default.
• W2596099863 cites W1970353818 @default.
• W2596099863 cites W1970460436 @default.
• W2596099863 cites W1970501840 @default.
• W2596099863 cites W1970527216 @default.
• W2596099863 cites W1970528730 @default.
• W2596099863 cites W1970706135 @default.
• W2596099863 cites W1971621147 @default.
• W2596099863 cites W1971763771 @default.
• W2596099863 cites W1971944856 @default.
• W2596099863 cites W1972173305 @default.
• W2596099863 cites W1972422715 @default.
• W2596099863 cites W1972546023 @default.
• W2596099863 cites W1973247222 @default.
• W2596099863 cites W1973470715 @default.
• W2596099863 cites W1973471035 @default.
• W2596099863 cites W1974018894 @default.
• W2596099863 cites W1974112332 @default.
• W2596099863 cites W1974448472 @default.
• W2596099863 cites W1975587028 @default.
• W2596099863 cites W1975995627 @default.
• W2596099863 cites W1976267307 @default.
• W2596099863 cites W1976282831 @default.
• W2596099863 cites W1976885142 @default.
• W2596099863 cites W1977010911 @default.
• W2596099863 cites W1977073662 @default.
• W2596099863 cites W1977634797 @default.
• W2596099863 cites W1978081589 @default.

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