Publication

Huntingtin-Associated Protein 1 in Mouse Hypothalamus Stabilizes Glucocorticoid Receptor in Stress Response

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Last modified
  • 05/14/2025
Type of Material
Authors
    Xingxing Chen, Wuhan University of Science and TechnologyNing Xin, Xuzhou Medical UniversityYongcheng Pan, Emory UniversityLouyin Zhu, Emory UniversityPeng Yin, Jinan UniversityQiong Liu, Emory UniversityWeili Yang, Jinan UniversityXingshun Xu, Soochow UniversityShihua Li, Jinan UniversityXiao-Jiang Li, Emory University
Language
  • English
Date
  • 2020-06-04
Publisher
  • Frontiers Media S.A.
Publication Version
Copyright Statement
  • © 2020 Chen, Xin, Pan, Zhu, Yin, Liu, Yang, Xu, Li and Li.
License
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 14
Start Page
  • 125
End Page
  • 125
Grant/Funding Information
  • This work was supported by National Institutes of Health (NIH) grant NS036232, the National Natural Science Foundation of China (Grant Nos. 81830032 and 31872779) and “Guangdong Key Laboratory of non-human primate models of brain diseases,” Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology (No. OHIC2019G02).
Abstract
  • Huntingtin-associated protein 1 (Hap1) was initially identified as a brain-enriched protein that binds to the Huntington’s disease protein, huntingtin. Unlike huntingtin that is ubiquitously expressed in the brain, Hap1 is enriched in the brain with the highest expression level in the hypothalamus. The selective enrichment of Hap1 in the hypothalamus suggests that Hap1 may play a specific role in hypothalamic function that can regulate metabolism and stress response. Here we report that Hap1 is colocalized and interacts with the glucocorticoid receptor (GR) in mouse hypothalamic neurons. Genetic depletion of Hap1 reduced the expression level of GR in the hypothalamus. Dexamethasone, a GR agonist, treatment or fasting of mice induced stress, resulting in increased expression of Hap1 in the hypothalamus. However, when Hap1 was absent, these treatments promoted GR reduction in the hypothalamus. In cultured cells, loss of Hap1 shortened the half-life of GR. These findings suggest that Hap1 stabilizes GR in the cytoplasm and that Hap1 dysfunction or deficiency may alter animal’s stress response.
Author Notes
Keywords
Research Categories
  • Biology, Cell
  • Biology, Genetics
  • Biology, Neuroscience

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