Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 129, Issue 9, Pages 3864-3876Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI122599
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Funding
- National Natural Science Foundation of China [81671301, 81471319, 81873788, 81622015, 81571042]
- National Clinical Key Specialty Construction Foundation of China
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The expression of the transmembrane protein 25 gene (Tmem25) is strongly influenced by glutamate ionotropic receptor kainate type subunit 4, and its function remains unknown. Here, we showed that TMEM25 was primarily localized to late endosomes in neurons. Electrophysiological experiments suggested that the effects of TMEM25 on neuronal excitability were likely mediated by N-methyl-D-aspartate receptors. TMEM25 affected the expression of the N-methyl-D-aspartate receptor NR2B subunit and interacted with NR2B, and both were colocalized to late endosome compartments. TMEM25 induced acidification changes in lysosome compartments and accelerated the degradation of NR2B. Furthermore, TMEM25 expression was decreased in brain tissues from patients with epilepsy and epileptic mice. TMEM25 overexpression attenuated the behavioral phenotypes of epileptic seizures, whereas TMEM25 downregulation exerted the opposite effect. These results provide some insights into TMEM25 biology in the brain and the functional relationship between TMEM25 and epilepsy.
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