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dc.contributor.authorKleppe, Runeen_US
dc.contributor.authorHerfindal, Larsen_US
dc.contributor.authorDøskeland, Stein Oveen_US
dc.date.accessioned2016-08-08T07:23:01Z
dc.date.available2016-08-08T07:23:01Z
dc.date.issued2015-10-22
dc.PublishedMarine Drugs 2015, 13(10):6505-6520eng
dc.identifier.issn1660-3397
dc.identifier.urihttps://hdl.handle.net/1956/12478
dc.description.abstractOkadaic acid (OA) and microcystin (MC) as well as several other microbial toxins like nodularin and calyculinA are known as tumor promoters as well as inducers of apoptotic cell death. Their intracellular targets are the major serine/threonine protein phosphatases. This review summarizes mechanisms believed to be responsible for the death induction and tumor promotion with focus on the interdependent production of reactive oxygen species (ROS) and activation of Ca2+/calmodulin kinase II (CaM-KII). New data are presented using inhibitors of specific ROS producing enzymes to curb nodularin/MC-induced liver cell (hepatocyte) death. They indicate that enzymes of the arachidonic acid pathway, notably phospholipase A2, 5-lipoxygenase, and cyclooxygenases, may be required for nodularin/MC-induced (and presumably OA-induced) cell death, suggesting new ways to overcome at least some aspects of OA and MC toxicity.en_US
dc.language.isoengeng
dc.publisherMDPIeng
dc.rightsAttribution CC BYeng
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/eng
dc.subjectmicrocystineng
dc.subjectokadaic acideng
dc.subjectnodularineng
dc.subjectcell deatheng
dc.subjectapoptosiseng
dc.subjectprotein phosphataseeng
dc.subjectinhibitoreng
dc.titleCell Death inducing microbial protein phosphatase inhibitors-mechanisms of actionen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2016-04-08T11:22:42Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2015 by the authors
dc.identifier.doihttps://doi.org/10.3390/md13106505
dc.identifier.cristin1282795


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Attribution CC BY
Except where otherwise noted, this item's license is described as Attribution CC BY