Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41419-018-1230-5
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dc.titleDR-region of Na + /K + ATPase is a target to treat excitotoxicity and stroke
dc.contributor.authorShi, M
dc.contributor.authorCao, L
dc.contributor.authorCao, X
dc.contributor.authorZhu, M
dc.contributor.authorZhang, X
dc.contributor.authorWu, Z
dc.contributor.authorXiong, S
dc.contributor.authorXie, Z
dc.contributor.authorYang, Y
dc.contributor.authorChen, J
dc.contributor.authorWong, P.T.H
dc.contributor.authorBian, J.-S
dc.date.accessioned2020-09-04T01:43:20Z
dc.date.available2020-09-04T01:43:20Z
dc.date.issued2019
dc.identifier.citationShi, M, Cao, L, Cao, X, Zhu, M, Zhang, X, Wu, Z, Xiong, S, Xie, Z, Yang, Y, Chen, J, Wong, P.T.H, Bian, J.-S (2019). DR-region of Na + /K + ATPase is a target to treat excitotoxicity and stroke. Cell Death and Disease 10 (1) : 6. ScholarBank@NUS Repository. https://doi.org/10.1038/s41419-018-1230-5
dc.identifier.issn2041-4889
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/174190
dc.description.abstractNa + /K + ATPase (NKA) is important in maintaining cellular functions. We found that loss of NKA activities in NKA?1 +/? mice is associated with increased susceptibility to ischemic injuries following transient middle cerebral artery occlusion (tMCAO). This is corroborated by the neuroprotective effects of an antibody raised against an extracellular DR region ( 897 DVEDSYGQQWTYEQR 911 , sequence number as in rat) of NKA? subunit (DR-Ab) in both preventive and therapeutic settings. DR-Ab protects cortical neurons against glutamate-induced toxicity by stimulating activities of NKA and Na + /Ca 2+ exchanger (NCX), which resulted in accelerated Ca 2+ extrusion. DR-Ab also enhanced the association between NKA and GluR2 and therefore reduced the internalization of both proteins from membrane induced by glutamate toxicity. The mechanism appears to involve suppression of GluR2 phosphorylation through PKC?/PICK pathway. Our data indicate that DR-region of NKA may be a novel therapeutic target for drug development for the treatment of ischemic stroke. © 2018, The Author(s).
dc.publisherNature Publishing Group
dc.sourceUnpaywall 20200831
dc.subjectadenosine triphosphatase (potassium sodium)
dc.subjectcalcium
dc.subjectglutamic acid
dc.subjectprotein interacting with protein kinase C
dc.subjectadenosine triphosphatase (potassium sodium)
dc.subjectAMPA receptor
dc.subjectantibody
dc.subjectglutamate receptor ionotropic, AMPA 2
dc.subjectglutamic acid
dc.subjectpeptide
dc.subjectsodium calcium exchange protein
dc.subjectanimal cell
dc.subjectanimal tissue
dc.subjectapoptosis
dc.subjectArticle
dc.subjectbrain cell culture
dc.subjectbrain tissue
dc.subjectcalcium cell level
dc.subjectcell membrane
dc.subjectcell viability
dc.subjectcerebrovascular accident
dc.subjectcomparative study
dc.subjectconfocal microscopy
dc.subjectcontrolled study
dc.subjectendocytosis
dc.subjectexcitotoxicity
dc.subjectimmunoprecipitation
dc.subjectinfarct volume
dc.subjectinternalization
dc.subjectmiddle cerebral artery occlusion
dc.subjectmouse
dc.subjectnerve cell plasticity
dc.subjectnerve excitability
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein phosphorylation
dc.subjecttime-lapse microscopy
dc.subjectWestern blotting
dc.subjectwhole cell patch clamp
dc.subjectanimal
dc.subjectbrain cortex
dc.subjectcerebrovascular accident
dc.subjectchemistry
dc.subjectdisease model
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectnerve cell
dc.subjectpathology
dc.subjectAnimals
dc.subjectAntibodies
dc.subjectCerebral Cortex
dc.subjectDisease Models, Animal
dc.subjectGlutamic Acid
dc.subjectMice
dc.subjectNeurons
dc.subjectPeptides
dc.subjectReceptors, AMPA
dc.subjectSodium-Calcium Exchanger
dc.subjectSodium-Potassium-Exchanging ATPase
dc.subjectStroke
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.contributor.departmentLIFE SCIENCES INSTITUTE
dc.description.doi10.1038/s41419-018-1230-5
dc.description.sourcetitleCell Death and Disease
dc.description.volume10
dc.description.issue1
dc.description.page6
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