Please use this identifier to cite or link to this item:
https://doi.org/10.1038/s41419-018-1230-5
DC Field | Value | |
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dc.title | DR-region of Na + /K + ATPase is a target to treat excitotoxicity and stroke | |
dc.contributor.author | Shi, M | |
dc.contributor.author | Cao, L | |
dc.contributor.author | Cao, X | |
dc.contributor.author | Zhu, M | |
dc.contributor.author | Zhang, X | |
dc.contributor.author | Wu, Z | |
dc.contributor.author | Xiong, S | |
dc.contributor.author | Xie, Z | |
dc.contributor.author | Yang, Y | |
dc.contributor.author | Chen, J | |
dc.contributor.author | Wong, P.T.H | |
dc.contributor.author | Bian, J.-S | |
dc.date.accessioned | 2020-09-04T01:43:20Z | |
dc.date.available | 2020-09-04T01:43:20Z | |
dc.date.issued | 2019 | |
dc.identifier.citation | Shi, 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.issn | 2041-4889 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/174190 | |
dc.description.abstract | Na + /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.publisher | Nature Publishing Group | |
dc.source | Unpaywall 20200831 | |
dc.subject | adenosine triphosphatase (potassium sodium) | |
dc.subject | calcium | |
dc.subject | glutamic acid | |
dc.subject | protein interacting with protein kinase C | |
dc.subject | adenosine triphosphatase (potassium sodium) | |
dc.subject | AMPA receptor | |
dc.subject | antibody | |
dc.subject | glutamate receptor ionotropic, AMPA 2 | |
dc.subject | glutamic acid | |
dc.subject | peptide | |
dc.subject | sodium calcium exchange protein | |
dc.subject | animal cell | |
dc.subject | animal tissue | |
dc.subject | apoptosis | |
dc.subject | Article | |
dc.subject | brain cell culture | |
dc.subject | brain tissue | |
dc.subject | calcium cell level | |
dc.subject | cell membrane | |
dc.subject | cell viability | |
dc.subject | cerebrovascular accident | |
dc.subject | comparative study | |
dc.subject | confocal microscopy | |
dc.subject | controlled study | |
dc.subject | endocytosis | |
dc.subject | excitotoxicity | |
dc.subject | immunoprecipitation | |
dc.subject | infarct volume | |
dc.subject | internalization | |
dc.subject | middle cerebral artery occlusion | |
dc.subject | mouse | |
dc.subject | nerve cell plasticity | |
dc.subject | nerve excitability | |
dc.subject | neuroprotection | |
dc.subject | nonhuman | |
dc.subject | priority journal | |
dc.subject | protein expression | |
dc.subject | protein phosphorylation | |
dc.subject | time-lapse microscopy | |
dc.subject | Western blotting | |
dc.subject | whole cell patch clamp | |
dc.subject | animal | |
dc.subject | brain cortex | |
dc.subject | cerebrovascular accident | |
dc.subject | chemistry | |
dc.subject | disease model | |
dc.subject | genetics | |
dc.subject | metabolism | |
dc.subject | nerve cell | |
dc.subject | pathology | |
dc.subject | Animals | |
dc.subject | Antibodies | |
dc.subject | Cerebral Cortex | |
dc.subject | Disease Models, Animal | |
dc.subject | Glutamic Acid | |
dc.subject | Mice | |
dc.subject | Neurons | |
dc.subject | Peptides | |
dc.subject | Receptors, AMPA | |
dc.subject | Sodium-Calcium Exchanger | |
dc.subject | Sodium-Potassium-Exchanging ATPase | |
dc.subject | Stroke | |
dc.type | Article | |
dc.contributor.department | PHARMACOLOGY | |
dc.contributor.department | LIFE SCIENCES INSTITUTE | |
dc.description.doi | 10.1038/s41419-018-1230-5 | |
dc.description.sourcetitle | Cell Death and Disease | |
dc.description.volume | 10 | |
dc.description.issue | 1 | |
dc.description.page | 6 | |
Appears in Collections: | Elements Staff Publications |
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