Year: 2021
Type: article
Abstract: Selenoprotein K (SELENOK), an endoplasmic reticulum (ER) resident protein, is regulated by dietary selenium and expressed at a relatively high level in neurons. SELENOK has been shown to participate in oxidation resistance, calcium (Ca2+) flux regulation, and the ER-associated degradation (ERAD) pathway in immune cells. However, its role in neurons has not been elucidated. Here, we demonstrated that SELENOK gene knockout markedly enhanced ER stress (ERS) and increased apoptosis in neurons. SELENOK gene knockout elicited intracellular Ca2+ flux and activated the m-calpain/caspase-12 cascade, thus inducing neuronal apoptosis both in vivo and in vitro. In addition, SELENOK knockout significantly reduced cognitive ability and increased anxiety in 7-month-old mice. Our findings reveal an unexpected role of SELENOK in regulating ERS-induced neuronal apoptosis.
Source: Redox Biology
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,450
Funders: National Natural Science Foundation of China, Natural Science Foundation of Guangdong Province, Shenzhen University, Shenzhen Fundamental Research Program, Shenzhen-Hong Kong Institute of Brain Science, National Institutes of Health, National Institute of General Medical Sciences, National Institute of Allergy and Infectious Diseases
OpenAlex ID: W3203400002