FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2014203494> ?p ?o ?g. }

• W2014203494 endingPage "22" @default.
• W2014203494 startingPage "16" @default.
• W2014203494 abstract "Nerve agent toxicity is primarily due to the synaptic build up of toxic levels of acetylcholine. The acute lethal effects of the nerve agents are generally attributed to respiratory failure caused by a combination of effects at both central and peripheral levels and are further complicated by copious secretions, muscle fasciculations, and convulsions. In addition to this, a range of non cholinergic effects have been observed. The development of effective treatment to block multiple effects resulting from nerve agent exposure is hampered by a limited understanding of the molecular changes responsible for their persistent effects. Excessive accumulation of acetylcholine leads to activation nicotinic and muscarinic acetylcholine receptors, these receptors activate diverse kind of cellular responses by distinct signaling pathways. Metabolism of cyclic nucleotides, membrane phospholipids, activation of a multitude of protein kinases and the induction of transcription factors are the key biochemical steps and pathways that have been investigated. This review will focus on the effects of nerve agents on signal transduction pathways; particularly, MAP kinases, protein kinase C isozymes, calcium calmodulin dependent protein kinase II (CaMKII) and on cytoskeletal proteins, calpain, and certain transcription factors and discusses how such changes may be involved in nerve agent induced neurotoxicity. Alterations in these key brain proteins could explain the neurological impairments following nerve agent exposure. A better understanding of the whole picture may lead to new pharmacological interventions aimed to improve or modulate those signal transduction pathways affected during nerve agent poisoning or associated pathologies that are responsible for neuronal disturbances." @default.
• W2014203494 created "2016-06-24" @default.
• W2014203494 creator A5052847966 @default.
• W2014203494 creator A5061359831 @default.
• W2014203494 date "2012-01-01" @default.
• W2014203494 modified "2023-10-10" @default.
• W2014203494 title "Multiple signal transduction pathways alterations during nerve agent toxicity" @default.
• W2014203494 cites W1489003835 @default.
• W2014203494 cites W1532805410 @default.
• W2014203494 cites W1563531877 @default.
• W2014203494 cites W1660120640 @default.
• W2014203494 cites W178343997 @default.
• W2014203494 cites W185143481 @default.
• W2014203494 cites W1967160570 @default.
• W2014203494 cites W1973327478 @default.
• W2014203494 cites W1974616331 @default.
• W2014203494 cites W1976568235 @default.
• W2014203494 cites W1978300562 @default.
• W2014203494 cites W1979406476 @default.
• W2014203494 cites W1982553044 @default.
• W2014203494 cites W1984173947 @default.
• W2014203494 cites W1988667044 @default.
• W2014203494 cites W1990735551 @default.
• W2014203494 cites W1991351596 @default.
• W2014203494 cites W1992254762 @default.
• W2014203494 cites W1995474789 @default.
• W2014203494 cites W2001162182 @default.
• W2014203494 cites W2001567826 @default.
• W2014203494 cites W2002175811 @default.
• W2014203494 cites W2007213375 @default.
• W2014203494 cites W2013426884 @default.
• W2014203494 cites W2015981968 @default.
• W2014203494 cites W2018379740 @default.
• W2014203494 cites W2019868620 @default.
• W2014203494 cites W2021170634 @default.
• W2014203494 cites W2022372459 @default.
• W2014203494 cites W2023629636 @default.
• W2014203494 cites W2024553493 @default.
• W2014203494 cites W2027693921 @default.
• W2014203494 cites W2029218246 @default.
• W2014203494 cites W2031022912 @default.
• W2014203494 cites W2036087996 @default.
• W2014203494 cites W2037155998 @default.
• W2014203494 cites W2038431896 @default.
• W2014203494 cites W2038496041 @default.
• W2014203494 cites W2043016952 @default.
• W2014203494 cites W2044282697 @default.
• W2014203494 cites W2046827859 @default.
• W2014203494 cites W2048466291 @default.
• W2014203494 cites W2048966030 @default.
• W2014203494 cites W2053089178 @default.
• W2014203494 cites W2054799772 @default.
• W2014203494 cites W2061380047 @default.
• W2014203494 cites W2063526770 @default.
• W2014203494 cites W2066148514 @default.
• W2014203494 cites W2071140879 @default.
• W2014203494 cites W2073456775 @default.
• W2014203494 cites W2081186222 @default.
• W2014203494 cites W2081787790 @default.
• W2014203494 cites W2086528889 @default.
• W2014203494 cites W2094587177 @default.
• W2014203494 cites W2103245870 @default.
• W2014203494 cites W2106088076 @default.
• W2014203494 cites W2108558950 @default.
• W2014203494 cites W2109674931 @default.
• W2014203494 cites W2124763951 @default.
• W2014203494 cites W2132985423 @default.
• W2014203494 cites W2137385309 @default.
• W2014203494 cites W2140872647 @default.
• W2014203494 cites W2145965566 @default.
• W2014203494 cites W2146376140 @default.
• W2014203494 cites W2154680573 @default.
• W2014203494 cites W2165543524 @default.
• W2014203494 cites W244606901 @default.
• W2014203494 cites W4232706823 @default.
• W2014203494 cites W4366345816 @default.
• W2014203494 cites W44788869 @default.
• W2014203494 cites W79984152 @default.
• W2014203494 doi "https://doi.org/10.1016/j.toxlet.2011.09.022" @default.
• W2014203494 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22001750" @default.
• W2014203494 hasPublicationYear "2012" @default.
• W2014203494 type Work @default.
• W2014203494 sameAs 2014203494 @default.
• W2014203494 citedByCount "22" @default.
• W2014203494 countsByYear W20142034942013 @default.
• W2014203494 countsByYear W20142034942014 @default.
• W2014203494 countsByYear W20142034942015 @default.
• W2014203494 countsByYear W20142034942016 @default.
• W2014203494 countsByYear W20142034942017 @default.
• W2014203494 countsByYear W20142034942018 @default.
• W2014203494 countsByYear W20142034942019 @default.
• W2014203494 countsByYear W20142034942020 @default.
• W2014203494 countsByYear W20142034942023 @default.
• W2014203494 crossrefType "journal-article" @default.
• W2014203494 hasAuthorship W2014203494A5052847966 @default.
• W2014203494 hasAuthorship W2014203494A5061359831 @default.
• W2014203494 hasConcept C126322002 @default.
• W2014203494 hasConcept C169760540 @default.

• next