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      14-3-3 Isoforms Differentially Regulate NFκB Signaling in the Brain After Ischemia-Reperfusion.

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          Abstract

          Mammalian 14-3-3 isoforms exist predominantly in the brain and are heavily involved in neurological diseases. However, the isoform-specific role of 14-3-3 proteins in the brain remains largely unclear. Here, we investigated the role of 14-3-3 isoforms in rat brains after transient middle cerebral artery occlusion and reperfusion. 14-3-3β, η, γ and ζ but not ε or τ were selectively upregulated in cerebral cortical neurons after ischemia-reperfusion (I/R). Selectively, 14-3-3β, γ and ζ were translocated from cytoplasm into the nuclei of neurons after I/R. 14-3-3 bound to p65 and suppressed p65 expression in N2a cells. In the brain, 14-3-3 could either colocalize with p65 in the nuclei of neurons or segregate from p65 expression in cortical neurons after I/R. All evidence together suggests that 14-3-3 isoforms are differentially induced to enter into the nuclei of neurons after I/R, which might regulate NFκB signaling directly or indirectly. Since 14-3-3 proteins are essential for cell survival and NFκB is a key transcriptional factor, our data suggest that the 14-3-3/p65 signaling pathway might be a potential therapeutic target for stroke.

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          Author and article information

          Journal
          Neurochem. Res.
          Neurochemical research
          Springer Nature America, Inc
          1573-6903
          0364-3190
          Aug 2017
          : 42
          : 8
          Affiliations
          [1 ] Department of Neurology, First Affiliated Hospital of SoocChow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, China.
          [2 ] Department of Neurology, Lianyungang Hospital affiliated with Xuzhou Medical College, Tongguan Road 182, Lianyungang, Jiangsu, China.
          [3 ] Department of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan, 430030, Hubei, China.
          [4 ] Department of Neurology, First Affiliated Hospital of SoocChow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, China. dwlsz8@163.com.
          [5 ] Department of Traumatic Surgery, Tong-ji Hospital, Tong-ji Medical College, Huazhong University of Science and Technology, Jie Fang Avenue 1095, Wuhan, 430030, Hubei, China. chenglayi@163.com.
          Article
          10.1007/s11064-017-2255-3
          10.1007/s11064-017-2255-3
          28424948
          a068aec1-332b-4065-9d90-f998271cb77f
          History

          Brain protection,BiFC,14-3-3 protein,Stroke,ShRNA,P65
          Brain protection, BiFC, 14-3-3 protein, Stroke, ShRNA, P65

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