PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8529864-8 1995 One of them is related to catalytic action of iron and ascorbate, while the other to an enzyme, possibly phospholipase A2, as has been suggested by some investigators. Iron 46-50 phospholipase A2 group IB Homo sapiens 105-121 9727376-10 1998 Exogenous C20:4, as well as PLA2 (in doses simulating Fe-induced deacylation) recapitulated Fe"s ceramide-generating effect. Iron 54-56 phospholipase A2 group IB Homo sapiens 28-32 9727376-10 1998 Exogenous C20:4, as well as PLA2 (in doses simulating Fe-induced deacylation) recapitulated Fe"s ceramide-generating effect. Iron 92-94 phospholipase A2 group IB Homo sapiens 28-32 22732705-0 2012 Differential participation of phospholipase A2 isoforms during iron-induced retinal toxicity. Iron 63-67 phospholipase A2 group IB Homo sapiens 30-46 1727652-6 1992 Another phospholipase A2 inhibitor, mepacrine, poorly inhibited both microsomal and pool-B"-promoted lipid peroxidation, but did block both iron-ascorbate-driven and ABAP-promoted lipid peroxidation. Iron 140-144 phospholipase A2 group IB Homo sapiens 8-24 29454663-1 2018 INTRODUCTION: Phospholipase A2-associated neurodegeneration (PLAN) is an autosomal recessive movement disorder with abnormal iron deposition in basal ganglia, substantial nigra and adjacent areas, and cerebellar atrophy. Iron 125-129 phospholipase A2 group IB Homo sapiens 14-30 1358548-0 1992 Effects of copper, iron and zinc on oedema formation induced by phospholipase A2. Iron 19-23 phospholipase A2 group IB Homo sapiens 64-80 1358548-6 1992 Copper, iron and zinc have an inhibitory effect on vascular permeability increase and paw oedema induced by PLA2. Iron 8-12 phospholipase A2 group IB Homo sapiens 108-112 1358548-8 1992 Copper and iron could have not only a direct effect on PLA2 but on enzymes of arachidonic acid cascade. Iron 11-15 phospholipase A2 group IB Homo sapiens 55-59 22732705-3 2012 The role of phospholipase A(2) (PLA(2)) during iron-induced retinal toxicity was investigated. Iron 47-51 phospholipase A2 group IB Homo sapiens 32-38 12813050-5 2003 PLA2 activity assessed by release of preloaded [3H]AA after treatment with AA+Fe was higher in the CYP2E1 expressing HepG2 cells. Iron 78-80 phospholipase A2 group IB Homo sapiens 0-4 22266337-2 2012 Neurodegeneration with brain iron accumulation (NBIA) involves several genetic disorders, two of which, aceruloplasminemia and neuroferritinopathy, are caused by mutations in genes directly involved in iron metabolic pathway, and others, such as pantothenate-kinase 2, phospholipase-A2 and fatty acid 2-hydroxylase associated neurodegeneration, are caused by mutations in genes coding for proteins involved in phospholipid metabolism. Iron 29-33 phospholipase A2 group IB Homo sapiens 269-285 16783378-0 2006 PLA2G6, encoding a phospholipase A2, is mutated in neurodegenerative disorders with high brain iron. Iron 95-99 phospholipase A2 group IB Homo sapiens 19-35 12813050-8 2003 PLA2 inhibitors also blocked mitochondrial damage in the CYP2E1-expressing HepG2 cells exposed to AA+Fe. Iron 101-103 phospholipase A2 group IB Homo sapiens 0-4 12813050-12 2003 These results suggest that release of stored calcium by AA+Fe, induced by lipid peroxidation, can initially activate calpain and PLA2 activity, that PLA2 activation is critical for a subsequent increased influx of extracellular Ca2+, and that the combination of increased PLA2 and calpain activity, increased calcium and oxidative stress cause mitochondrial damage, that ultimately produces the rapid toxicity of AA+Fe in CYP2E1-expressing HepG2 cells. Iron 59-61 phospholipase A2 group IB Homo sapiens 129-133 12511994-1 2002 Damages to liposomal membranes resulted from intensification of lipid peroxidation with iron ions in the presence of ascorbate or treatment with the membrane disintegrator tetrachloromethane led to activation of phospholipase A2, which depended on the enzyme localization in liposomes. Iron 88-92 phospholipase A2 group IB Homo sapiens 212-228