2. Academic Validation
  3. UBQLN4 regulates seizures by promoting the proteasomal degradation of GluN2B

UBQLN4 regulates seizures by promoting the proteasomal degradation of GluN2B

  • Neurobiol Dis. 2025 Oct 15:215:107090. doi: 10.1016/j.nbd.2025.107090.
Wang Jing 1,  Yan Xia 1,  Zhang Hui 1,  Wang Xuefeng 1,  Xu Demei 2,  Peng Xi 3,  Wang Liang 4
Affiliations

Affiliations

  • 1 Department of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Major Neurological and Mental Disorders, Chongqing Key Laboratory of Neurology, Chongqing, China.
  • 2 Department of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Major Neurological and Mental Disorders, Chongqing Key Laboratory of Neurology, Chongqing, China. Electronic address: tiankongfeiyu204@163.com.
  • 3 Department of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: px5523@126.com.
  • 4 Department of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Major Neurological and Mental Disorders, Chongqing Key Laboratory of Neurology, Chongqing, China. Electronic address: wang0128_0@163.com.
PMID: 40930427 DOI: 10.1016/j.nbd.2025.107090
Abstract

Ubiquilin 4 (UBQLN4) is an important molecule that regulates protein degradation through the ubiquitin-proteasome pathway. This study found that UBQLN4 expression is significantly reduced in a chronic epilepsy mouse model induced by kainic acid, primarily localized in neurons and widely distributed at excitatory post-synapses. Experiments involving adeno-associated virus-mediated overexpression or knockdown of UBQLN4 indicate that a reduction in UBQLN4 increases susceptibility to and severity of epilepsy, while its overexpression has a protective effect. Mechanistic studies show that UBQLN4 regulates the degradation of the N-Methyl d-Aspartate 2B Subunit (GluN2B) via the Proteasome pathway, thereby affecting synaptic function. This research reveals the critical role of UBQLN4 in epilepsy and provides a potential new target for the treatment of epilepsy.

Keywords

Epilepsy; GluN2B; Proteasome pathway; UBQLN4.

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